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:
Flu-like symptoms, such as fever and chills
A new or changed heart murmur, which is the heart sounds made by blood rushing through your heart
Fatigue
Aching joints and muscles
Splenomegaly
Stiff neck
Delirium
Night sweats
Shortness of breath
Chest pain on breathing
Swelling in legs or abdomen
Conjunctival hemorrhage
Pallor
Gallops
Rales
Cardiac arrhythmia
Pericardial rub

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

5. 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
CXR of a patient with tricuspid valve endocarditis
Multiple cavitating lung nodules due to septic pulmonary emboli.

6. Petechiae
Janeway lesions

7. Splinter hemorrhage
Osler node

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
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
Intravenous drug use
Fever of 38°C or higher
Vascular phenomenon:
Major arterial emboli
Septic pulmonary infarcts
Mycotic aneurysm
ICH
Janeway lesions
Conjunctival hemorrhage
Immunologic phenomenon:
Glomerulonephritis
Osler nodes
Roth spots
Rheumatoid factor
A definitive clinical diagnosis is based on:
2 major criteria
1 major criterion and 3 minor criteria
5 minor criteria

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

11. Prosthetic valve endocarditis
which presents in a subacute fashion similar to NVE.
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 R> L atrium
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%).

12. IVDA infective endocarditis
Diagnosis in IV drug users requires a high index of suspicion.
2/3 of patients have no previous history of heart disease or murmur.
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 3/4 demonstrate chest radiographic abnormalities.
S aureus is the most common (>50% of cases) 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. Differential Diagnoses
Thrombotic nonbacterial endocarditis
Vasculitis
Temporal arteritis
Marantic endocarditis
Connective tissue disease
Fever of unknown origin (FUO)
Intra-abdominal infections
Septic pulmonary infarction
Antiphospholipid Syndrome
Atrial Myxoma
Cardiac Neoplasms, Primary
Lyme Disease
Polymyalgia Rheumatica
Reactive Arthritis
Systemic Lupus Erythematosus

14. 3 sets may be drawn over 30 minutes (with separate venipunctures)
Diagnostic work up:
Criterion standard for diagnosis of (IE) is the documentation of a continuous bacteremia (>30 min in duration) on blood culture results
3 sets may be drawn over 30 minutes (with separate venipunctures)
Culture-negative infective endocarditis
Vasculitis
Prior antibiotic therapy
Fungal infections
Atypical organisms
CBC (Leukocytosis)
ESR (Elevated in 90%)
BUN
Coagulation Profile
RF (+50%)
Proteinuria
Hematuria
3-5 sets of blood cultures over 24 hours

15. 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, 20% in PVE.
TEE
Can detect the NVE vegetations of in %.
Sensitivity is greater than 90% for PVE.
Can visualize vegetations of Tricuspid valve in > 90%.
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

16. 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 (in patients with RF)
Empiric antibiotic therapy is chosen based on the most likely infecting organisms.

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

18. 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 include:
CHF refractory to
standard medical therapy
Fungal IE
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 aortic valve IE
Paravalvular abscess and intracardiac fistula

19. 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 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

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