1. INFECTIVE ENDOCARDITIS
Dr. M. A. SOFI
MD; FRCP (London); FRCPEdin; FRCSEdin

2. Fever possibly low-grade and intermittent 90%.
Infective endocarditis (IE) is defined as an infection of the endocardial surface of the heart, which may include one or more heart valves, the mural endocardium, or a septal defect.
Signs and symptoms
Fever possibly low-grade and intermittent %.
Heart murmurs 85%
Petechiae: Common, but nonspecific, finding
Subungual (splinter) hemorrhages: Dark-red, linear lesions in the nail beds
Osler nodes: Tender subcutaneous nodules usually found on the distal pads of the digits
Janeway lesions: Non-tender maculae on the palms and soles
Roth spots: Retinal hemorrhages with small, clear centers; rare

3. Other signs of IE include the following:
Splenomegaly
Stiff neck
Delirium
Paralysis, hemiparesis, aphasia
Conjunctival hemorrhage
Pallor
Gallops
Rales
Cardiac arrhythmia
Pericardial rub
Pleural friction rub

4. Multiple cavitating lung nodules due to septic pulmonary emboli.
Chest radiograph of a patient with tricuspid valve endocarditis due to S. aureus
Patients with IE may have involvement of other organs:
Metastatic infection (eg, vertebral osteomyelitis),
Embolic events (eg, focal neurologic deficits, renal infarct, splenic infarct).
Systemic immune reaction (eg, glomerulonephritis).
In right-sided endocarditis, septic pulmonary emboli may be seen
Multiple cavitating lung nodules due to septic pulmonary emboli.

5. Petechiae
Janeway lesions

6. Splinter hemorrhage
Osler node

7. Native valve endocarditis
The symptoms of early subacute native valve endocarditis are usually subtle and nonspecific; they include the following:
Syndromes similar to rheumatic fever, such as fever, dull sensorium, headaches
Abdominal symptoms, such as right upper quadrant pain, vomiting, postprandial distress, appendicitis-like symptoms
Low-grade fever: Absent in 3-15% of patients
Anorexia
Weight loss
Influenza-like syndromes
Polymyalgia-like syndromes
Pleuritic pain

8. Diagnosis
The Duke diagnostic criteria, are generally used to make a definitive diagnosis of IE. The criteria combine the clinical, microbiologic, pathologic, and echocardiographic characteristics of a specific case
Blood culture criteria for IE:
Typical microorganism for infective endocarditis from two separate blood cultures
Blood cultures persistently positive for one of these organisms, from cultures drawn more than 12 hours apart
Three or more separate blood cultures drawn at least 1 hour apart
Echocardiographic criteria for IE
Oscillating intracardiac mass on a valve or on supporting structures, in the path of regurgitant jets, or on implanted material.
Myocardial abscess
Development of partial dehiscence of a prosthetic valve
New-onset valvular regurgitation

9. Minor criteria for IE include the following:
Predisposing heart condition or intravenous drug use
Fever of 38°C or higher
Vascular phenomenon:
Major arterial emboli
Septic pulmonary infarcts
Mycotic aneurysm
Intracranial hemorrhage
Conjunctival hemorrhage
Janeway lesions
Immunologic phenomenon:
Glomerulonephritis
Osler nodes
Roth spots
Rheumatoid factor
Positive blood culture results not meeting major criteria or serologic evidence of active infection with an organism consistent with IE
Echocardiogram results consistent with IE but not meeting major echocardiographic criteria
A definitive clinical diagnosis can be made based on the following:
2 major criteria
1 major criterion and 3 minor criteria
5 minor criteria

10. Native valve endocarditis: Main underlying causes of NVE
RHD (30% of NVE) - Primarily involves the mitral valve followed by the aortic valve
Degenerative heart disease:
Calcific aortic stenosis due to a bicuspid valve
Marfan syndrome
Syphilitic disease
Mitral valve prolapse with an associated murmur (20% of NVE)
Congenital heart disease
(15% of NVE) - Underlying etiologies include:
Patent ductus arteriosus
Ventricular septal defect
Tetralogy of Fallot
Native or surgical high-flow lesion.
Approximately 70% of infections in NVE are caused by Streptococcus species, including S viridans, Streptococcus bovis, and enterococci. Staphylococcus species cause 25% of cases and generally demonstrate a more aggressive acute course.

11. Prosthetic valve endocarditis
Early PVE, which presents shortly after surgery, has a different bacteriology and prognosis than late PVE, which presents in a subacute fashion similar to NVE.
Pericardial tamponade
Peripheral emboli to the CNS and elsewhere.
Early PVE may be caused by:
S aureus and S epidermidis. These nosocomially acquired organisms are often methicillin-resistant ( MRSA).
Late disease is commonly caused by streptococci.
Overall, CoNS are the most frequent cause of PVE (30%).
Aortic valve prostheses infection is particularly associated with:
local abscess and fistula formation
Valvular dehiscence.
This may lead to:
Shock
Heart failure
Heart block
Shunting of blood to the rght atrium

12. IVDA infective endocarditis
Diagnosis in IV drug users can be difficult and requires a high index of suspicion.
2/3 of patients have no previous history of heart disease or murmur on admission.
A murmur may be absent in those with tricuspid disease.
Pulmonary manifestations may be prominent in patients with tricuspid infection:
1/3 have pleuritic chest pain, and three quarters demonstrate chest radiographic abnormalities.
S aureus is the most common (< 50% of cases) etiologic organism in patients with IVDA IE.
MRSA accounts for an increasing portion of S aureus infections and has been associated with previous hospitalizations, long-term addiction, and non-prescribed antibiotic use.
Groups A, C, and G streptococci and enterococci are also recovered from patients with IVDA IE.

13. Nosocomial/healthcare-associated infective endocarditis
Endocarditis may be associated with:
Central or peripheral IV catheters
Pacemakers and defibrillators
Hemodialysis shunts
Hyperalimentation lines
These patients tend to have significant comorbidities, more advanced age, and predominant infection with S aureus.
The mortality rate is high in this group.  
The organisms that cause NIE/HCIE obviously are related to the type of underlying bacteremia. The gram-positive cocci (S aureus, CoNS, enterococci, nonenterococcal streptococci) are the most common pathogens. Fungal endocarditis is found in IV drug users and ICU patients who receive broad-spectrum antibiotics. Blood cultures are often negative, and diagnosis frequently is made after microscopic examination of large emboli.

14. Differential Diagnoses
Thrombotic nonbacterial endocarditis
Vasculitis
Temporal arteritis
Marantic endocarditis
Connective tissue disease
Fever of unknown origin (FUO)
Intra-abdominal infections
Septic pulmonary infarction
Tricuspid regurgitation
Antiphospholipid Syndrome
Atrial Myxoma
Cardiac Neoplasms, Primary
Endocarditis
Lyme Disease
Polymyalgia Rheumatica
Reactive Arthritis
Systemic Lupus Erythematosus

15. Diagnostic work up:
The criterion standard test for diagnosing infective endocarditis (IE) is the documentation of a continuous bacteremia (>30 min in duration) based on blood culture results
25% of patients with staphylococcal bacteremia and 23% of those with catheters as the primary focus have evidence of IE based on transesophageal echocardiography (TEE) findings, in the absence of clinical and transthoracic echocardiography (TTE) findings.
25% of S aureus bloodstream infections (BSIs) represent IE or metastatic infections
S aureus to produce an endotheliosis, the presence of a continuous bacteremia does not necessarily imply an infected valvular vegetation
Clue to continuous bacteremia /IE is the presence of S aureus bacteriuria associated with hematuria

16. Diagnostic work up: CBC (Leukocytosis in acute stage)
Criterion standard for diagnosis of (IE) is the documentation of a continuous bacteremia (>30 min in duration) on blood culture results
CBC (Leukocytosis in acute stage)
ESR (Elevated in 90%)
BUN
Coagulation Profile
RF (+50%)
Proteinuria
Hematuria
3-5 sets of blood cultures over 24 hours
3 sets may be drawn over 30 minutes (with separate venipunctures)
Culture-negative infective endocarditis
Vasculitis
Prior antibiotic therapy
Fungal infections
Atypical organisms

17. Echocardiography: Echocardiography has become diagnostic method of choice. The diagnosis of IE can never be excluded based on negative echocardiogram .
TTE sensitivity is 60% for NVE valvular lesions
TTE sensitivity is 20% in PVE.
TEE can detect the NVE vegetations of in %.
The TEE sensitivity is greater than 90% for PVE.
TEE can visualize vegetations of the Tricuspid valve in more than 90% of pacemaker IE, compared with less than the 50% achieved by TTE.
Echocardiography can predict embolic complications of IE.
Predictors of systemic embolization include:
Large valvular vegetations (>10 mm in diameter)
Multiple vegetations
Mobile but pedunculated vegetations
Prolapsing vegetations
Echocardiography is also highly useful for detecting abscesses

18. Treatment
The major goals of therapy for infective endocarditis (IE) are:
Eradicate the infectious agent from the thrombus
Intra cardiac and extra cardiac consequences of IE.
Surgical intervention.
Emergency care: Correct diagnosis & stabilization
General Measures:
Treatment of congestive heart failure
Oxygen
Hemodialysis (may be required in patients with RF)
Empiric antibiotic therapy is chosen based on the most likely infecting organisms.

19. Treatment
Native valve endocarditis (NVE): Penicillin G wih gentamicin for synergistic coverage of streptococci
Patients with IVdrug use have been treated with nafcillin and gentamicin to cover for methicillin-sensitive staphylococci.
Prosthetic valve endocarditis (PVE) may be caused by MRSA or coagulase-negative staphylococci (CoNS)
Culture-negative NVE is usually treated with vancomycin and gentamicin
Patients with culture-negative PVE are usually given vancomycin and gentamicin, targeting enterococcal or CoNS infections

20. Approximately 15-25% of patients with IE eventually require surgery
Approximately 15-25% of patients with IE eventually require surgery. Indications for surgical intervention in patients with NVE are as follows:
CHF refractory to standard medical therapy
Fungal IE (except that caused by Histoplasma capsulatum)
Persistent sepsis after 72 hours of appropriate antibiotic Rx
Recurrent septic emboli, especially after 2 weeks of antibiotic treatment
Rupture of an aneurysm of the sinus of Valsalva
Conduction disturbances caused by a septal abscess
Kissing infection of the anterior mitral leaflet in patients with IE of the aortic valve
Paravalvular abscess and intracardiac fistula almost always require surgical intervention

21. Prevention of IE:15-25% cases of IE are due to procedures that produce bacteremia
Consider prophylaxis in procedures involving:
Manipulation of gingival tissue or the periapical region of teeth.
Infected musculoskeletal tissue or skin including incision and drainage of an abscess
Prophylaxis is no longer routinely recommended for GI procedures.
High risk patients include:
Presence of prosthetic heart valve
History of endocarditis
Cardiac transplant recipients who develop cardiac valvulopathy
Congenital heart disease with a high-pressure gradient lesion

22. THANK
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