Infective endocarditis
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| Infective endocarditis Classification and external resources | |
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| Mitral valve vegetations in a patient with bacterial endocarditis. | |
| ICD-10 | I33. |
| ICD-9 | 421 |
| DiseasesDB | 4224 |
| MedlinePlus | 001098 |
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| MeSH | D004696 |
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Related Key Words and Synonyms: Infective endocarditis, IE, subacute bacterial endocarditis, acute bacterial endocarditis, fungal endocarditis, nosocomial infective endocarditis, NIE, intravenous drug abuse endocarditis, intravenous drug abuse infective endocarditis, IVDA endocarditis, IVDA IE, prosthetic valve endocarditis, PVE, pacemaker endocarditis, PM infective endocarditis, PM IE, endocardial infection, native valve endocarditis, NVE, HACEK infection, bloodstream infection, marantic endocarditis
Overview
Endocarditis is an inflammation of the inner layer of the heart, the endocardium. The most common structures involved are the heart valves.
Endocarditis can be classified by etiology as either non-infective or infective, depending on whether a microorganism is the source of the problem.
Traditionally, infective endocarditis has been clinically divided into acute and subacute (because the patients tend to live longer in subacute as opposed to acute) endocarditis. This classifies both the rate of progression and severity of disease. Thus subacute bacterial endocarditis (SBE) is often due to streptococci of low virulence and mild to moderate illness which progresses slowly over weeks and months, while acute bacterial endocarditis (ABE) is a fulminant illness over days to weeks, and is more likely due to Staphylococcus aureus which has much greater virulence, or disease-producing capacity.
This terminology is now discouraged. The terms short incubation (meaning less than about six weeks), and long incubation (greater than about six weeks) are preferred.
Infective endocarditis may also be classified as culture-positive or culture-negative. Culture-negative endocarditis is due to micro-organisms that require a longer period of time to be identified in the laboratory. Such organisms are said to be 'fastidious' because they have demanding growth requirements. Some pathogens responsible for culture-negative endocarditis include Aspergillus species, Brucella species, Coxiella burnetii, Chlamydia species, and HACEK bacteria.
Finally, the distinction between native-valve endocarditis and prosthetic-valve endocarditis is clinically important. Prosthetic-valve endocarditis constitutes 10-20% of cases of endocarditis. The greatest risk is during the first 6 months after valve surgery. Staphylococcus epidermidis is the most common cause. The infection often extends into the anulus and cardiac tissues.
Patients who inject narcotics intravenously may introduce infection which will travel to the right side of the heart. In other patients without a history of intravenous exposure, endocarditis is more frequently left-sided.
Non-infective endocarditis
Non-infective or marantic endocarditis is rare. A form of sterile endocarditis is termed Libman-Sacks endocarditis; this form occurs more often in patients with lupus erythematosus and the antiphospholipid syndrome. Non-infective endocarditis may also occur in patients with cancer, particularly mucinous adenocarcinoma.
Infective endocarditis
Given the poor vascular supply of the heart valves, entrance of infection fighting components of the bloodstream (such as white blood cells) are reduced. So if an organism (such as bacteria) establishes a foothold in the valves, the bodies ability to fight the infection inside the valve structures is reduced.
Normally, blood flows smoothly through these valves. If they have been damaged (for instance in rheumatic fever) the trauma of non-laminar flow can increase the risk of infection.
Historical Background of Endocarditis
- 1554: Earliest report of endocarditis in medical books
- 1669: Accurately described tricuspid valve endocarditis
- 1646: Described unusual "outgrowths" from autopsy of patient with endocarditis; detected murmurs by placing hand on patient's chest
- 1708: Described unusual structures in entrance of aorta
- 1715: Described abnormality in aortic valve and mitral valve
- 1749: Described valvular lesions
- 1769: Linked infectious disease and endocarditis; observed association with the spleen
- 1784: Accurately drew intracardiac abnormalities
- 1797: Showed relationship between rheumatism and heart disease
- 1799: Described inflammatory process associated with endocarditis
- 1806: Described unusual structures in heart as "vegetations," syphilitic virus as causative agent of endocarditis, and theory of antiviral treatment of endocarditis
- 1809: Indicated vegetations were not "outgrowths" or "buds" but particles adhering to heart wall
- 1815: Elucidated inflammatory processes associated with endocarditis
- 1816: Invented cylindrical stethoscope to listen to heart murmurs; dismissed link between venereal disease and endocarditis
- 1832: Confirmed Laennec's observations
- 1835-40: Named endocardium and endocarditis; described symptoms; prescribed herbal tea and bloodletting as treatment regimen; described link between acute rheumatoid arthritis and endocarditis
- 1852: Described consequences of embolization of vegetations throughout body. Described cutaneous nodules (named "Osler's nodes" by Libman)
- 1858-71: Examined fibrin vegetation associated with endocarditis by microscope; coined term "embolism;" discussed role of bacteria, vibrios, and micrococci in endocarditis
- 1861: Confirmed Virchow's theory on emboli
- 1862: Described granulations or foreign elements in blood and valves, which were motile and resistant to alkalis
- 1868-70: Described infected arterial blood as originating from heart; proposed scarlet fever as cause of endocarditis
- 1869: Established "parasites" on skin transported to heart and attached to endocardium; named "mycosis endocardii"
- 1872: Detected microorganisms in vegetations of endocarditis
- 1878: All cases of endocarditis were infectious in origin
- 1878: Combined experimental physiology and infection to produce animal model of endocarditis in rabbit; noted valve had to be damaged before bacteria grafted onto valve
- 1878: Micrococci enter vessels that valves were fitted into; valves exposed to abnormal mechanical attacks over long period created favorable niche for bacterial colonization
- 1879: Virchow's student; employed early animal model of endocarditis
- 1879: Proposed etiology of endocarditis was based on infectious model and treatment should focus on eliminating "parasitic infection"
- 1880: Working with Pasteur, proposed use of routine blood cultures
- 1881-86: Believed endocarditis could appear during various infections; noted translocation of respiratory pathogen from pulmonary lesion to valve through blood
- 1883: Believed microorganisms were result, not cause, of endocarditis
- 1884: Named disease "infective endocarditis"
- 1886: Demonstrated various bacteria introduced to bloodstream could cause endocarditis on valve that had previous lesion
- 1885: Synthesized work of others relating to endocarditis
- 1899: Described streptococcal, staphylococcal, pneumococcal, and gonococcal endocarditis
- 1903: First described "endocarditis lenta"
- 1909: Credited by Osler as first to observe cutaneous nodes (named "Osler's nodes" by Libman) in patients with endocarditis
- 1909: Analyzed 150 cases of endocarditis and published diagnostic criteria relating to signs and symptoms
- 1910: Described initial classification scheme to include "subacute endocarditis," with clinical signs/symptoms; absolute diagnosis required blood cultures
- 1981: Described Beth Israel criteria based on strict case definitions
- 1994: New criteria utilizing specific echocardiographic findings
- 1995: Antibiotic treatment of adults with infective endocarditis caused by streptococci, enterococci, staphylococci, and HACEK (a) microorganisms
- 1996: Modified Duke Criteria to allow serologic diagnosis of Coxiella burnetii
- 1997: Guidelines for preventing bacterial endocarditis
- 1997: Suggested modifications to Duke criteria for clinical diagnosis of native valve and prosthetic valve endocarditis: analysis of 118 pathologically proven cases
- 1998: Guidelines for antibiotic treatment of streptococcal, enterococcal, and staphylococcal endocarditis
- 1998: Antibiotic treatment of infective endocarditis due to viridans streptococci, enterococci, and other streptococci; recommendations for surgical treatment of endocarditis
- 2000: Updated and modified Duke Criteria
- 2002: Duke Criteria to include a molecular diagnosis of causal agents
- 2001-3: Described etiology of Bartonella spp., Tropheryma whipplei, and Coxiella burnetii in endocarditis
Epidemiology and Demographics
The incidence of IE is approximately 2-4 cases per 100,000 persons per year worldwide. This rate has not changed in the past 5-6 decades.
IE may occur in a person of any age. The frequency is increasing in elderly individuals, with 25-50% of cases occurring in those older than 60 years of age. The occurrence of IE is 3 times more common in males than in females.
Risk Factors
Adults and children with underlying cardiac conditions placing them at highest risk for adverse outcomes of infective endocarditis (IE) including those with:
- Prosthetic cardiac valve or prosthetic cardiac valve repair
- Previous infective endocarditis
- Congenital heart disease (CHD) associated with
- Unrepaired cyanotic CHD, including palliative shunts and conduits
- Completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure
- Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization)
- Cardiac transplantation patients who develop cardiac valvulopathy
Screening
Among those patients at high risk, careful monitoring should be undertaken to detect the early development of complications such as:
- Valvular dysfunction, usually insufficiency of the mitral or aortic valves;
- Myocardial or septal abscesses
- Congestive heart failure
- Metastatic infection
- Embolic phenomenon
Pathophysiology & Etiology
As previously mentioned, altered blood flow around the valves is a risk factor for the development of endocarditis. The valves may be damaged congenitally, from surgery, by auto-immune mechanisms, or simply as a consequence of old age. The damaged part of a heart valve becomes covered with a blood clot, a condition known as non-bacterial thrombotic endocarditis (NBTE).
In a healthy individual, a bacteremia (where bacteria get into the blood stream through a minor cut or wound) would normally be cleared quickly with no adverse consequences. If a heart valve is damaged and covered with thrombus, these structures can provide a nidus for bacteria to attach themselves and an infection can be established.
The bacteremia is often caused by dental procedures, such as a cleaning or extraction of a tooth. It is important that a dentist or a dental hygienist therefore be told of any heart problems before beginning the procedure. Prophylactic antibiotics are administered to patients with certain heart conditions as a precaution.
Another cause of infective endocarditis is a scenario in which an excess number of bacteria enter the bloodstream. Colorectal cancer, serious urinary tract infections, and IV drug use can all introduce large numbers of such bacteria. When a large burden of bacteria are introduced, a normal heart valve may be infected. A more virulent organism (such as Staphylococcus aureus, but see below for others) is often responsible for infecting a normal valve.
Infections of the tricuspid valve and less frequently the pulmonic valve tend to occur in intravenous drug users given the high pathogen burden from their introduction in the vein. The diseased valve is most commonly affected when there is a pre-existing disease. In rheumatic heart disease this is the aortic valve and the mitral valves, on the left side of the heart.
Complications of endocarditis can occur as a result of the locally destructive effects of the infection. These complications include perforation of valve leaflets, perforation of fistula between blood vessels or cardiac chambers, abscesses and disruption of conduction system.
Natural History and Complications
Complications of infective endocarditis include the following:
- Cardiac
- Murmur
- New aortic diastolic murmur suggests dilatation of the aortic annulus or eversion, rupture, or fenestration of an aortic leaflet
- Sudden onset of loud mitral pansystolic murmur suggests rupture of chorda tendineae or fenestration of a mitral valve leaflet
- Congestive heart failure
- Cardiac rhythm disturbances
- Occasionally, pericarditis
- Cutaneous
- Petechiae of the conjunctiva, oropharynx, skin, and legs
- Linear subungual splinter haemorrhages of the lower or middle nail bed
- Oslers nodes
- Janeway lesions
- Musculoskeletal
- Myalgias
- Arthralgias
- Arthritis
- Low back pain
- Rheumatoid factor in up to 50% of patients with endocarditis for > 6 wk
- Clubbing of fingers in < 15% of patients
- Ocular
- Petechial hemorrhages,
- Flame-shaped hemorrhages,
- Roth's spots,
- Cotton-wool exudates in the retina
- Embolic
- Significant arterial emboli occur in 30%–50% of patients, causing the following:
- Stroke
- Monocular blindness
- Acute abdominal pain, ileus, and melena
- Pain and gangrene in the extremities
- CNS emboli are common
- Coronary emboli, often asymptomatic, can cause myocardial infarction
- Pulmonary emboli common in right-sided endocarditis, causing pulmonary infarcts or focal pneumonitis
- Splenic
- Splenomegaly in 15%–30% of patients
- Splenic infarcts in up to 40% of patients
- Splenic abscesses in ~ 5% of patients
- Renal
- Microscopic hematuria in ~ 50% of patients
- Embolic renal infarction
- Diffuse membranoproliferative glomerulonephritis
- Mycotic aneurysms
Occur in any artery in 2%–8% of patients, causing the following:
- Pain or headache
- Pulsatile mass
- Fever
- Sudden expanding hematoma
- Signs of major blood loss
- Neurologic
- Neurologic complications occur in 25%–40% of cases
- Strokes caused by cerebral embolisms in ~ 15% of cases, causing the following:
- Altered level of consciousness
- Seizures
- Fluctuating focal neurologic signs
- Cerebral aneurysms occur in 1%–5% of cases, causing the following:
- Headache
- Focal signs
- Acute intracerebral or subarachnoid hemorrhage caused by rupture
- Mild meningeal irritation resulting from slow leakage
- Brain abscesses may occur in acute endocarditis caused by Staphylococcus aureus
- Seizures
Diagnosis
In general, a patient should fulfill the Duke Criteria[1] in order to establish the diagnosis of endocarditis.
As the Duke Criteria relies heavily on the results of echocardiography, research has addressed when to order an echocardiogram by using signs and symptoms to predict occult endocarditis among patients with intravenous drug abuse[1][1][1] and among non drug abusing patients [1][1]. Unfortunately, this research is over 20 years old and it is possible that changes in the epidemiology of endocarditis and bacteria such as staphylococcus make the following estimates incorrectly low.
Among patients who do not use illicit drugs and have a fever in the emergency room, there is a less than 5% chance of occult endocarditis. Mellors [1] in 1987 found no cases of endocarditis nor of staphylococcal bacteremia among 135 febrile patients in the emergency room. The upper confidence interval for 0% of 135 is 5%, so for statistical reasons alone, there is up to a 5% chance of endocarditis among these patients. In contrast, Leibovici [1] found that among 113 non-selected adults admitted to the hospital because of fever there were two cases (1.8% with 95%CI: 0% to 7%) of endocarditis.
Among patients who do use illicit drugs and have a fever in the emergency room, there is about a 10% to 15% prevalence of endocarditis. This estimate is not substantially changed by whether the doctor believes the patient has a trivial explanation for their fever[1]. Weisse[1] found that 13% of 121 patients had endocarditis. Marantz [1] also found a prevalence of endocarditis of 13% among such patients in the emergency room with fever. Samet [1] found a 6% incidence among 283 such patients, but after excluding patients with initially apparent major illness to explain the fever (including 11 cases of manifest endocarditis), there was a 7% prevalence of endocarditis.
Among patients with staphylococcal bacteremia (SAB), one study found a 29% prevalence of endocarditis in community-acquired SAB versus 5% in nosocomial SAB[1]. However, only 2% of strains were resistant to methicillin and so these numbers may be low in areas of higher resistance.
Common Causes
Many types of organism can cause infective endocarditis. These are generally isolated by blood culture, where the patient's blood is removed, and any growth is noted and identified.
Alpha-haemolytic streptococci, that are present in the mouth will often be the organism isolated if a dental procedure caused the bacteraemia.
If the bacteraemia was introduced through the skin, such as contamination in surgery, during catheterisation, or in an IV drug user, Staphylococcus aureus is common.
A third important cause of endocarditis is Enterococci. These bacteria enter the bloodstream as a consequence of abnormalities in the gastrointestinal or urinary tracts. Enterococci are increasingly recognized as causes of nosocomial or hospital-acquired endocarditis. This contrasts with alpha-haemolytic streptococci and Staphylococcus aureus which are causes of community-acquired endocarditis.
Some organisms, when isolated, give valuable clues to the cause, as they tend to be specific.
- Candida albicans, a yeast, is associated with IV drug users and the immunocompromised. Fungal endocarditis accounts for 5% of cases of native endocarditis and 10% of cases of prosthetic valve endocarditis. A diagnosis of fungal endocarditis is difficult, because many patients are afebrile with a normal white blood cell count (WBC). The fungus is often difficult to culture, and blood cultures typically negative. Fungal infections often result in large vegetations, systemic embolization, myocardial invasion, and are extremely resistant to medical therapy. Early surgical intervention is warranted because medical mortality approaches 100% Anti-fungal therapy for life is required.
- Pseudomonas species, which are very resilient organisms that thrive in water, may contaminate street drugs that have been contaminated with drinking water. P. aeruginosa can infect a child through foot punctures, and can cause both endocarditis and septic arthritis.[1]
- Streptococcus bovis and Clostridium septicum, which are part of the natural flora of the bowel, are associated with colonic malignancies. When they present as the causative agent in endocarditis, it usually call for a concomitant colonoscopy due to worries regarding hematogenous spread of bacteria from the colon due to the neoplasm breaking down the barrier between the gut lumen and the blood vessels which drain the bowel.[1]
- HACEK organisms are a group of bacteria that live on the dental gums, and can be seen with IV drug abusers who contaminate their needles with saliva. Patients may also have a history of poor dental hygiene, or pre-existing valvular disease.[1]
Differential Diagnosis of Risk Factors for or Causes of Infective endocarditis
| Cardiovascular | • Asymmetric septal hypertrophy • Calcific aortic stenosis • Cardiac catheterization • Cardiac surgery • Congenital Heart Disease • Mitral valve prolapse • Prosthetic heart valve • Septal defects • Valve disease • Previous bacterial endocarditis • Rheumatic Heart Disease • Sclerotherapy • Cardiac myxoma |
| Chemical / poisoning | No underlying causes |
| Dental | • Dental extractions • Dental implants • Root canals • |
| Dermatologic | • Skin infection • |
| Drug Side Effect | • IV drug use • |
| Ear Nose Throat | • Adenoidectomy • |
| Endocrine | No underlying causes |
| Environmental | No underlying causes |
| Gastroenterologic & Genito-Uriner | • Biliary tract surgery • Cystoscopy • Endoscopic retrograde cholangiopancreatography • Urethral dilation • Prostatic surgery • |
| Genetic | • Marfan's Syndrome • |
| Hematologic | No underlying causes |
| Iatrogenic | No underlying causes |
| Infectious Disease | • Diphtheria • Staphylococcus epidermidis • Staphylococcus aureus • Streptococcus bovis • Viridans streptococci • Group A streptococcus • Gram negative rods • Enterococuss • Candida • Tuberculosis • Salmonellosis |
| Musculoskeletal / Ortho | No underlying causes |
| Neurologic | No underlying causes |
| Nutritional / Metabolic | No underlying causes |
| Obstetrics & Gynecology | • Childbirth • |
| Oncologic | No underlying causes |
| Opthalmologic | No underlying causes |
| Overdose / Toxicity | No underlying causes |
| Psychiatric | No underlying causes |
| Pulmonary | • Respiratory infection • Respiratory tract procedures • |
| Renal / Electrolyte | No underlying causes |
| Rheum / Immune / Allergy | • Juvenile rheumatoid arthritis • Polymyalgia rheumatica • Acute rheumatic fever • Polyarteritis nodosa • Systemic lupus erythematosus • Antiphospholipid antibody syndrome • |
| Trauma | No underlying causes |
| Miscellaneous | • Surgical systemic-pulmonary shunts and conduits • |
History and Symptoms
A. Subacute Bacterial Endocarditis (SBE)
- Insidious onset
- Fever
- Sweats
- Weakness
- Myalgias
- Arthralgias
- Malaise
- Anorexia
- Fatigue
- Splenomegaly, clubbing, and Oslers nodes in long-standing SBE
B. Acute Bacterial Endocarditis
C. Endocarditis Associated with Parenteral Drug Use
- High fevers, chills, rigors, malaise, cough, and pleuritic chest pain
- Septic pulmonary emboli causing sputum production, hemoptysis, and signs suggesting pneumonia
- Cardiac murmurs
- Tricuspid insufficiency
- Metastatic infections
- Neurologic manifestations
- Peripheral emboli
D. Prosthetic Valve Endocarditis
- Occurs in 1%–2% of cases at 1 yr and in 4%–5% of cases at 4 yr after implantation
- Infection of perivalvular tissues
- Valvular dysfunction
- Myocardial abscesses
- Fever
- Petechiae, Roth's spots, Osler's nodes, Janeway lesions
- Emboli
Physical Examination
Vital Signs
A fever will likely be present. Rigors may be present.
Skin
- Petechiae 10 - 40%
- Splinter haemorrhage 5 - 15%
- Oslers nodes 7 - 10% (tender subcutaneous nodules in pulp of digits)
- Janeway lesion 6 - 10% (erythematous, nontender lesions on palm or sole)
Eyes
Ear Nose and Throat
In patients in whom there is new acute onset of aortic regurgitation, bobbing of the uvula may be present.
Heart
- Heart Murmurs: 80 - 85%
Lungs
Signs of heart failure may present
Abdomen
- Abdominal pain may be present due to mesenteric embolization or ileus
- Splenomegaly may be found in 15-30% patients. Left upper quadrant (LUQ) pain may be present as a result of a splenic infarct from embolization
- Flank pain may be present as a result of an embolus to the kidney
Extremities
- Janeway lesions (painless hemorrhagic cutaneous lesions on the palms and soles)
- Gangrene of fingers may occur
- The fingers may show splinter haemorrhages
- Osler's nodes (painful subcutaneous lesions in the distal fingers)
Neurologic
Septic emboli may result in stroke and focal neurologic findings
Intracranial hemorrhage may occur
Symptoms Frequency
- Fever 80 - 85%, often spiking
- Chills 42 - 75%
- Anorexia 25 - 55%
- Malaise 25 - 40%
- Weight loss 25 - 35%
- Back pain
- Stroke may be present in 10 - 15% of patients as a result of cerebral embolization
- Chest pain may be present as a result of embolzation in the coronary artery. The infarcts are usually not transmural. Pulmonary emboli, often septic, occur in 75% of patients with tricuspid endocarditis
- Abdominal pain may be present due to mesenteric embolization or ileus
- Blindness may be present due to retinal embolization in 3% of patients
Laboratory Findings
An elevated erythrocyte sedimentation rate is present
A marked leukocytosis is present
A positive serum rheumatoid factor may be present (in approximately 50% of patients with subacute disease). It becomes negative after successful treatment.
The serum BUN and Cr may be elevated if glomerulonephritis is present
Urinalysis
Glomerulonephritis may be present
Electrocardiogram
There is no spesific EKG changes for diagnosis of Infective Endocarditis. EKG may help to detect the 10% of patients who develop a conduction delay during Infective Endocarditis by documenting an increased PR interval.
Chest X Ray
There are no specific chest x-ray findings specific for the diagnosis of endocarditis. Non specific findings would include findings of congestive heart failure.
MRI and CT
- A CT scan of the head should be obtained in patients who exhibit CNS symptoms or findings consistent with a mass effect (eg, macroabscess of the brain).
Echocardiography
Echocardiography is useful for risk stratification. Although the data are inconsistent, evidence suggests that vegetation size can predict embolic complications. In general, transthoracic echocardiography (TTE) is adequate for diagnosis of infective endocarditis in cases where cardiac structures-of-interest are well visualized.
Specific situations where transesophageal echocardiography (TEE) is preferred over TTE include the presence of a prosthetic valvular device, suspected periannular complications, children with complex congenital cardiac lesions, patients with S. Aureus caused bacteremia and pre-existing valvular abnormalities that make TTE interpretation more difficult (e.g. calcific aortic stenosis).
The transthoracic echocardiogram has a sensitivity and specificity of approximately 65% and 95% if the echocardiographer believes there is 'probabable' or 'almost certain' evidence of endocarditis[1][1].
Aims of echocardiography
- Determine the presence, location and size of vegetations
- Assess the damage to the valve apparatus and determine the haemodynamic effects.
- The dimensions and function of the ventricles.
- Identify any abscess formation
- Need for surgical intervention.
Echocardiographic features
- Irregular echogenic mass attached to valve leaflet
- attachment of the vegetation is on the upstream side of the valve leaflet
- independent movement of the mass (chaotic)
- minimum size of the vegetation identifiable on trans thoracic echocardiography is 3mm and by transoesophageal route is 2mm.
- With treatment and time, the vegetation shrinks and can get fibrosed or calcified - may not disappear completely.
- Large vegetations occur with fungal endocarditis or staph. aureus endocarditis.
- the haemodynamical effect is mostly due to regurgitation as a result of valve destruction.
Local complications
- Abscess
- Fistula
- Perforation
- Prosthetic dehiscence
When to do trans esophageal echocardiogram?
- Prosthetic valve endocarditis
- Poor trans thoracic views
- continuing sepsis in spite of adequate antibiotic therapy
- new PR prolongation
- No signs of endocarditis on trans thoracic echocardiography, but high clinical suspicion.
- Video 1: 2 D Echo shows Mitral Valve Vegetation,
- Video 2: 2 D Echo shows Aortic and Mitral Valve Vegetations
- Video 3: 2D Echo Tricuspid Valve Vegetation
- Fungal Endocarditis 1
- Fungal Endocarditis 2
- Fungal Endocarditis 3
- Fungal Endocarditis 4
- Fungal Endocarditis 5
Other Imaging Findings
- Various radionuclide scans using, for example, gallium Ga 67–tagged white cells and indium In 111–tagged white cells, have proven to be of little use in diagnosing IE.
Radionuclide scans of the spleen are useful to help rule out a splenic abscess, which is a cause of bacteremia that is refractory to antibiotic therapy.
Pathology
In acute phase
- Aneurysms
- Infected thrombi or vegetations
- Valve ulcers or erosions
- Rupture of chordaes
- Endocardial jet lesions
- Flail leaflets or cusps
- Abcess formation (annular and ring)
In chronic phase
- Perforations
- Nodular calcifications
- Tissue defects of valves
- Fibrosis of valves
Gross Pathology
Images shown in this section are courtesy of Professor Peter G. Anderson D.V.M. PhD, and published with permission.
© PEIR, University of Alabama at Birmingham, Department of Pathology
 Thrombotic Nonbacterial Endocarditis: (Gross) An excellent example of thrombi on aortic valve. |
 Thrombotic Nonbacterial Endocarditis: (Gross) Mitral valve lesion appears that have been present for at least several days. |
 Bacterial Endocarditis: (Gross) Perforated aortic valve cusp is shown. |
 Thrombotic Nonbacterial Endocarditis: (Gross) Aortic valve with two small vegetations. |
 Thrombotic Nonbacterial Endocarditis: (Gross) Mitral valve thrombi in chorda. |
 (Gross) A very good example of focal necrotizing lesions in distal portion of digit associated with bacterial endocarditis |
 Bacterial Endocarditis: (Gross) A lesion on non-coronary cusp of aortic valve. |
 Bacterial Endocarditis: (Gross) An excellent view of mitral scarring due to rheumatic fever healing infectious lesion. |
 Bacterial Endocarditis: (Gross) Aortic valve prosthesis ring infection extending into left atrium. |
Bacterial Endocarditis: (Gross) An excellent close-up view of mitral valve vegetations |
 Bacterial Endocarditis: (Gross) vegetations on mitral valve and left atrial endocardium due to actinomycosis |
 Bacterial Endocarditis: (Gross) An excellent image of vegetation on aortic valve |
 Bacterial Endocarditis: (Gross) An excellent image of vegetations on mitral valve evidence of rheumatic scarring |
 Thrombotic Nonbacterial Endocarditis: (Gross) Mitral valve, an excellent example |
 Thrombotic Nonbacterial Endocarditis: (Gross) Mitral valve: an excellent image, identical to acute rheumatic lesion |
 Verrucous Nonbacterial Endocarditis: (Gross) An excellent example of an infant heart |
 Purpura of cerebrum, cerebellum and brain stem in 36 years old female with Cushing syndrome and bacterial endocarditis caused by Staphylococcus aureus |
 Spleen infarct: (Gross) A typical small infarct with necrotic central portion (originated from infected marantic endocarditis on aortic and mitral valves) |
 Kidney infarct: (Gross) A natural color close-up and excellent image of yellow infarct marantic endocarditis on aortic and mitral valves |
 Thrombotic Nonbacterial Endocarditis Infected: (Gross) Natural color of pulmonary valve. An excellent example of patient with multiple myeloma |
 Thrombotic Non Bacterial Endocarditis: (Gross) Natural color of pulmonary valve. |
 Thrombotic Non Bacterial Endocarditis: (Gross) Natural color and good example of tricuspid valve lesions |
 Disseminated intravascular coagulation in endocarditis; tricuspid valve showing NBTE in DIC |
 Eye: Bacterial Endocarditis complicated as petechiae. Septic emboli to conjunctiva |
Treatment
High dose antibiotics are administered by the intravenous route to maximize diffusion of antibiotic molecules into vegetation(s) from the blood filling the chambers of the heart. This is necessary because neither the heart valves nor the vegetations adherent to them are supplied by blood vessels. Antibiotics are continued for a long time, typically two to six weeks. Specific drug regimens differ depending on the classification of the endocarditis as acute or subacute (acute necessitating treating for Staphylococcus aureus with oxacillin or vancomycin in addition to gram-negative coverage). Fungal endocarditis requires specific anti-fungal treatment, such as amphotericin B.[1]
Surgical removal of the valve is necessary in patients who fail to clear micro-organisms from their blood in response to antibiotic therapy, or in patients who develop cardiac failure resulting from destruction of a valve by infection. A removed valve is usually replaced with an artificial valve which may either be mechanical (metallic) or obtained from an animal such as a pig; the latter are termed bioprosthetic valves.[1]
Infective endocarditis is associated with a 10-25% mortality.
Pharmacotherapy
Effective treatment requires identification of the etiologic agent and determination of its antimicrobial susceptibility.
Antibiotic therapy for subacute or indolent disease can be delayed until results of blood cultures are known; in fulminant infection or valvular dysfunction requiring urgent surgical intervention, begin empirical antibiotic therapy promptly after blood cultures have been obtained.
For prosthetic valve endocarditis, treatment should be continued for 6–8 weeks.
Acute Pharmacotherapies
Penicillin-Susceptible Viridans and Other Nonenterococcal Streptococci[1]
The minimum inhibitory concentration [MIC] <0.2 µg/ml
- Penicillin G: preferred regimen
Dose: 12–18 million units I.V. daily in divided doses q. 4 hour for 4 weeks
- Penicillin G + gentamicin or ceftriaxone: preferred regimen
Dose: penicillin G, 12–18 million units I.V. daily in divided doses q. 4 hour for 4 weeks; gentamicin, 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hour for 2 weeks (peak serum concentration should be ~ 3 µg/ml and trough concentrations < 1 µg/ml); ceftriaxone, 2 g I.V. daily as a single dose for 2 weeks
- Vancomycin: for patients with history of penicillin hypersensitivity
Dose: 30 mg/kg I.V. daily in divided doses q. 12 hour for 4 weeks
Relatively Penicillin-Resistant Streptococci[1]
A- MIC 0.2–0.5 µg/ml
- Penicillin G + gentamicin: preferred regimen
Dose: penicillin G, 20–30 million units I.V. daily in divided doses q. 4 hour for 4 weeks; gentamicin, 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hr for 2 wk (peak serum concentration should be ~ 3 µg/ml and trough concentrations < 1 µg/ml)
B- MIC > 0.5 µg/ml
- Penicillin G + gentamicin: preferred regimen
Dose: penicillin G, 20–30 million units I.V. daily in divided doses q. 4 hour for 4 week; gentamicin, 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hour for 4 week (peak serum concentration should be ~ 3 µg/ml and trough concentrations < 1 µg/ml)
- Vancomycin: regimen for patients with history of penicillin hypersensitivity
Dose: 30 mg/kg I.V. daily in divided doses q. 12 hour for 4 weeks
Enterococci[1]
- Penicillin G + gentamicin: preferred regimen
Dose: penicillin G, 20–30 million units I.V. daily in divided doses q. 4 hr for 4–6 weeks; gentamicin, 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hour for 4–6 weeks (peak serum concentration should be ~ 3 µg/ml and trough concentrations < 1 µg/ml)
Dose: ampicillin, 12 g I.V. daily in divided doses q. 4 hour for 4–6 weeks; gentamicin, dose as above
- Vancomycin + gentamicin: regimen for patients with history of penicillin hypersensitivity
Dose: vancomycin, 30 mg/kg I.V. daily in divided doses q. 12 hour for 4–6 weeks; gentamicin, dose as above
Staphylococci (Methicillin Susceptible) in the Absence of Prosthetic Material[1]
- Nafcillin or oxacillin + gentamicin (optional): preferred regimen
Dose: nafcillin or oxacillin, 12 g I.V. daily in divided doses q. 4 hour for 4–6 weeks; gentamicin, 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hr for 3–5 days (peak serum concentration should be ~ 3 µg/ml and trough concentrations <1 µg/ml)
- Cefazolin + gentamicin (optional): alternative regimen for patients with history of penicillin hypersensitivity
Dose: cefazolin, 12 g I.V. daily in divided doses q. 4 hour for 4–6 weeks; gentamicin, dose as above
- Vancomycin: alternative regimen for patients with history of penicillin hypersensitivity
Dose: 30 mg/kg I.V. daily in divided doses q. 12 hr for 4–6 weeks
Staphylococci (Methicillin Resistant) in the Absence of Prosthetic Material[1]
Dose: 30 mg/kg I.V. daily in divided doses q. 12 hour for 4–6 weeks
Staphylococci (Methicillin Susceptible) in the Presence of Prosthetic Material[1]
- Nafcillin or oxacillin + rifampin + gentamicin
Dose: nafcillin or oxacillin, 12 g I.V. daily in divided doses q. 4 hour for 6–8 weeks; rifampin, 300 mg p.o., q. 8 hour for 6–8 weeks; gentamicin (administer during the initial 2 weeks), 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hour for 2 weeks
Staphylococci (Methicillin Resistant) in the Presence of Prosthetic Material[1]
Dose: vancomycin, 30 mg/kg I.V. daily in divided doses q. 12 hour for 6–8 weeks; rifampin, 300 mg p.o., q. 8 hour for 6–8 weeks; gentamicin (administer during the initial 2 weeks), 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hour for 2 weeks