Infective Endocarditis Flashcards
DF of Infective Endocarditis
Infective endocarditis (IE) is an infection of the endocardial surface of the heart. The
intracardiac effects of this infection include severe valvular insufficiency, which may lead to
intractable congestive heart failure and myocardial abscesses
Classification of Infective endocarditis
– depending on the type of valve affected
1. Native valve endocarditis (NVE): endocarditis that may develop on natural valve. The
affected valve may be damaged or normal.
2. Prosthetic valve endocarditis: is when the endocarditis develops on prosthetic/’artificial’ valve.
3. Endocarditis in intravenous drug abuser (IVDA).
There is a marked rise in cases of prosthetic valve endocarditis and endocarditis in IV drug abusers in different parts of the world. However Native valve endocarditis is the commonest
type of Infective endocarditis in Ethiopia and other developing countries.
The classic clinical presentation and clinical course of IE has been characterized as either acute or subacute
4. Acute Infective endocarditis: frequently involves healthy valves. It is a rapidly progressive illness with destruction of valvular structures.
5. Subacute Infective endocarditis: typically affects only previously damaged valves. The course is insidious even in untreated cases which may extend over many months
Etiologic agent of Infective endocarditis
1-Streptococcus viridans: is a bacterium which is a normal flora of the oral cavity. It accounts for approximately 50-60% of cases of subacute infective endocarditis.
2-Group D streptococci: the source for this bacterium is the gastrointestinal or genitourinary tract. Most cases infective endocarditis due to this organism is subacute.
3- S. aureus: is the leading cause of Prosthetic valve endocarditis (PVE), acute infective endocarditis and endocarditis in IV drug abusers. Approximately 35-60.5% of staphylococcal bacteremia is complicated by infective endocarditis. In more than half of cases endocarditis due to S. aureus occurs in the absence of underlying valvular disease. Mortality rate may range 40-50%
4- Coagulase-negative S. aureus: it accounts for approximately 30% of PVE cases, fewer than 5% of NVE cases. It causes subacute disease
5- HACEK organisms (i.e., Haemophilus species, Actinobacillus, actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella species) .These group of organisms usually cause subacute disease. It accounts for approximately 5% of infective endocarditis.
6- Fungus: Mostly frequently cause subacute disease. Candida albicans is the commonest fungal etiology.
Pathophysiology
–All cases of infective endocarditis develop from a commonly shared process:
1. Bacteremia (nosocomial or spontaneous) that delivers the organisms to the valve’s surface
2. Adherence of the organisms to valvular structures
3. Eventual invasion of the valvular leaflets and formation of vegetations.
Clinical Features of Subacute infective endocarditis
–A. Subacute infective endocarditis
The patient suspected of SBE should be asked about invasive procedures that may be causing bacteremia. Most subacute disease caused by S.viridans is related to dental disease.
The symptoms of early subacute NVE usually are subtle and nonspecific.
SBE is suggested by a history of a slowly progressive process characterized by fever,
fatigue, anorexia, back pain, and weight loss.
Less common developments are a cerebrovascular accident or congestive heart failure.
When appropriate therapy is delayed for weeks or months, additional clinical features,
embolic or immunological in origin, develop
–Embolic manifestations of infective endocarditis include:
o Acute meningitis with sterile spinal fluid
o Hemiplegia due to embolization in the distribution of the middle cerebral artery
o Renal regional infarcts producing painless hematuria
o Splenic infarction
o Unilateral blindness caused by occlusion of a retinal artery
o Myocardial infarction resulting from embolization to a coronary artery.
– Common Physical findings in SBE:
1-Fever: most patients have low grade fever; however 3-15% of patients with SBE may have normal or subnormal temperature.
2-Murmurs: the vast majority of patients have detectable heart murmurs (99% of cases). The absence of a murmur should cause clinicians to reconsider the diagnosis of IE. The major exception is right-sided infective endocarditis, in which only one third of cases have a detectable murmur.
3-The peripheral lesions of subacute infective endocarditis are observed in only approximately 20% of patients as compared to 85% in the preantibiotic era.
4-Petechiae are the most common peripheral lesions. They may occur on the palpebral conjunctivae, the dorsa of the hands and feet, the anterior chest and abdominal walls, the oral mucosa, and the soft palate.
5-Subungual hemorrhages (i.e., splinter hemorrhages) are linear and red lesions that do not extend for the entire length of the nail.
6-Clubbing of fingers and toes may be seen. It primarily occurs in those patients who have an extended course of untreated infective endocarditis.
7-Arthritis associated with subacute infective endocarditis is asymmetrical and limited to 1-3 joints.
8-Splenomegaly is observed more commonly in patients with long-standing subacute disease. It may persist long after successful therapy.
9-Osler nodes are small tender nodules that range in color from red to purple and are located primarily in the pulp spaces of the terminal phalanges of the fingers and toes, soles of the feet, and the thenar and hypothenar eminences of the hands.
Clinical Features of Acute infective endocarditis
1-Roth spots are retinal hemorrhages with pale centers. The Litten sign representscottonwool exudates.
2-Murmurs are present in nearly two third of patients with acute infective endocarditis.
The most common type is murmur aortic regurgitation. Because of the rapid onset, the left ventricle does not have a chance to dilate. In this situation, the classic findings of increased pulse pressure that are seen in chronic AR are absent.
3- Janeway lesions are irregular erythematous and painless macules (1-4 mm in diameter). They most often are located on the thenar and hypothenar eminences of the hands and feet. They usually represent an infectious vasculitis of acute infective endocarditis resulting from S. aureus infection.
4-Acute septic monoarticular arthritis in patients with acute infective endocarditis most often is caused by S aureus infection.
5-Purulent meningitis may be observed in patients with acute infective endocarditis , as compared to the aseptic type observed in patients with subacute disease.
explain Right-sided infective endocarditis , DF , Clinical manifestations ,LABORATORY MANIFESTATIONS ,Diagnosis
–DF :is associated with a very low rate of congestive heart
failure and valvular perforation.
NB! Pulmonary infarcts may result from emboli of right-sided infective endocarditis
-Clinical manifestations :
Fever > 95
Arthralgias and/or myalgias 25-45
Murmur > 85
Splenomegaly 25-60
Splinter hemorrhages 20-40
Roth’s spots < 5
Osler’s nodes 10-25
Janeway lesions < 5
Clubbing 10-20
Clinically apparent emboli 25-45
Neurologic manifestations 20-40
-LABORATORY MANIFESTATIONS :
Anemia 70-90
Leukocytosis 20-30
Proteinuria 50-65
Microscopic hematuria 30-50
Elevated serum creatinine level 10-20
Elevated erythrocyte sedimentation rate >90
Rheumatoid factor 50
Circulating immune complexes 65-100
Decreased serum complement level 5-40
–Diagnostic work up:
- Lab Studies:
1. Blood Culture :
1.1 The gold standard test for the diagnosis of infective endocarditis is the documentation of a continuous bacteremia (>30 min in duration) through blood
culture.
1.2 For making diagnosing SBE draw 3-5 sets of blood cultures , at 3 different sites , over 24 hours.
1.3 This detects 92-98% of cases in patients who have not received antibiotics recently.
1.4 In the case of Acute infective endocarditis, 3 sets may be drawn over 30 minutes (with separate venipunctures) to document a continuous bacteremia.
2. Echocardiography
2.1 Has become the indirect diagnostic method of choice, especially in patients who present with a clinical picture of infective endocarditis but who have nondiagnostic blood cultures.
2.2 The diagnosis of infective endocarditis can never be excluded by a negative echocardiogram.
3. Other Tests:
3.1 Electrocardiography may detect the 10% of patients who develop a conduction delay during infective endocarditis by documenting an increasing P-R interval.
4. Rheumatoid factor becomes positive in 50% of patients with subacute disease. It becomes negative after successful treatment
explain The Duke Criteria for the Clinical Diagnosis of Infective Endocarditis
-there is major and minor criteria :
1-Major Criteria :
1. Positive blood culture: for typical microorganism that causes infective endocarditis from two separate blood cultures. ( Viridans streptococci, Streptococcus bovis, HACEK group, or Community-acquired Staphylococcus aureus or enterococci in the absence of a primary focus )
2. Positive echocardiogram:
2.1 Definitive vegetation ( oscillating intracardiac mass on valve or supporting structures )
2.2 Abscess
2.3 New partial dehiscence of prosthetic valve
2.4 New valvular regurgitation (increase or change in preexisting murmur not sufficient)
2-Minor Criteria :
2.1 Predisposition: predisposing heart condition or IV drug abuse
2.2 Fever >38.0 oC.
2.3 Embolic phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions
2.4 Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots, rheumatoid factor
2.5 Microbiologic evidence: positive blood culture but not meeting major criterion.
2.6 Echocardiogram: consistent with infective endocarditis but not meeting major criterion
–Definitive Diagnosis can be made by documentation of:
Two major criteria or
One major and three minor criteria or
Five minor criteria allows a clinical diagnosis of definite endocarditis.
Treatment
–All patients should be treated in the hospital to allow adequate monitoring of the development of complications and the response to the antibiotic therapy.
1-General measures:
1.1Diet: No special diets are recommended for patients with endocarditis; however, if the patient has congestive heart failure, sodium-restriction may be necessary.
1.2 Activity: Activity limitations are determined by the severity of illness, complications (e.g., stroke), and the presence of significant congestive heart failure.
2-Medical Treatment:The major goals of therapy for infective endocarditis are
Eradicating the infectious agent from the thrombus
Treating the complications of valvular infection
1. Eradicating the infectious agent from the thrombus
- Antibiotics remain the mainstay of treatment for IE. In the setting of acute IE, antibiotic therapy should be instituted as soon as possible to minimize valvular damage. Three to five sets of blood cultures should be obtained within 60-90 minutes, followed by the infusion of the appropriate antibiotic regimen.
- By necessity, the initial antibiotic choice is empiric, determined by clinical history and physical examination.
- In the case of subacute IE, treatment may be safely delayed until cultures and
sensitivities are available. Waiting does not increase the risk of complications in this form of the disease.
- Eradicating bacteria from the fibrin-platelet thrombus is extremely difficult..
- Intravenous administration is the preferred to ensure reliable serum therapeutic levels.
- The antibiotics should be bactericidal and are should be administered at higher dose for prolonged period of time.
1.1 Empirical antibiotic treatment :
NVE of sub acute nature:
- Crystalline penicillin 3-4 million IU IV every 4 hours for 4- 6 weeks plus
- Gentamicin 1mg/kg ( 80 mg ) IV TID for 2 weeks plus
1.2 Prosthetic Valve endocarditis:
Vancomycin 1gm IV BID for 6 weeks Plus
Gentamicin 1mg/kg ( 80 mg ) IV TID for 2 weeks plus
Refampicin 300 mg PO /TID for 6 weeks
1.3 Acute Infective endocarditis where S.aureus is suspected: E.g. hospital acquired infection
Naficillin 1.5-2gm IV every 4 hours OR Vancomycin 1gm IV BID for 6 weeks Plus
Gentamicin 1mg/kg (80 mg) IV TID for 2 weeks
2. Dealing with the complications of valvular infection. The latter includes both the intracardiac and extracardiac consequences of infective endocarditis.
2.1 Mild congestive heart failure resulting from valvular insufficiency or myocarditis may be managed with standard medical therapy for CHF.
2.1 Although thrombosis is a key element of infective endocarditis, anticoagulation with heparin or Warfarin is controversial, and it should be avoided.
–Surgical Treatment: Approximately 15-25% of patients with IE eventually require surgery , Indication for Surgery:
Acute AR with severe Heart failure
Fungal endocarditis
Mobile vegetation > 10mm in size.
Evidence of valve ring or myocardial abscess
Recurrent embolization despite adequate antibiotic therapy
Poor response to antibiotics
Prosthetic valve dysfunction associated with CHF
Valve ring Abscess near a prosthetic valve
