This document provides information about endocarditis, including: - Endocarditis is an inflammation of the inner lining of the heart and heart valves. It is commonly caused by a heart valve infection from microorganisms entering the bloodstream. - It is classified as either acute or subacute based on symptoms and causative organisms. Common causative organisms include streptococci, staphylococci, and enterococci. - Risk factors include age over 50, pre-existing heart conditions, IV drug use, and dental procedures. Diagnosis involves blood cultures, echocardiogram, and application of the Modified Duke Criteria. Treatment involves antibiotics targeting the causative organism along with possible surgery

1. ENDOCARDITIS
BY
Mr.APOLLO JAMES, M.PHARM.,
ASSOC PROFESSOR,
DEPT.OF PHARMACY PRACTICE
NANDHA COLLEGE OF PHARMACY, ERODE

2. Definition- Endocarditis
• Endocarditis is an inflammation of the endocardium, the
membrane lining the chambers of the heart and covering
the cusps of the heart valves.
• More commonly, endocarditis refers to infection of the heart
valves by various microorganisms.
• Although it typically affects native valves, it also may
involve non-valvular areas or implanted mechanical
devices (e.g., mechanical heart valves).

3. Classification
ACUTE
• high fevers and systemic
toxicity.
• Virulent bacteria, such as
Staphylococcus aureus,
frequently
• If untreated, death may
occur within days to
weeks.
SUB ACUTE
• more indolent and it is
caused by less-invasive
organisms, such as
viridans streptococci,
• usually occurring in
preexisting valvular heart
disease

4. ETIOLOGY
Streptococci (60–80%)
• Viridans streptococci 30–40
• Other streptococci 15–25
Staphylococci 20–35
• Coagulase positive (10–27%)
• Coagulase negative 1–3
Enterococci 5–18
Gram-negative aerobic bacilli
1.5–13
Fungi 2–4
Miscellaneous bacteria <5
Mixed infections 1–2
• “Culture negative” <5–24
• HACEK: The group of
bacteria including
Haemophilus parainfluenzae,
Haemophilus aphrophilus,
Actinobacillus
actinomycetemcomitans,
Cardiobacterium hominis,
Eikenella corrodens, and
Kingella kingae

5. RISK FACTORS
• Older than 50 years
• Presence of prosthetic valves
• Valve replacement surgery
• IVDA
• Diabetes
• Long term hemodialysis
• Poor Dental Hygiene
• Complex cyanotic congenital heart disease (e.g., single-
ventricle states)
• Surgically constructed systemic pulmonary shunts or conduits
• Acquired valvular dysfunction (e.g., rheumatic heart disease)
• Hypertrophic cardiomyopathy
• Mitral valve prolapse with regurgitation

6. Pathophysiology
Hematogenous spread
Turbulent blood flow
Endothelial surface of heart damage
Platelet and fibrin deposition
Non bacterial thrombotic endocarditis
Bacteremia(Dental, Gastro, Urologic, Gynecological)
Vegetation of fibrin, platelet and bacteria forms
Local destruction, embolisation, Hematogenous spread, Antibody response

7. CLINICAL MANIFESTATION
Symptoms
• The patient may complain of fever, chills, weakness,
dyspnea, night sweats, weight loss, and/or malaise.
Signs
• Fever is common, as is a heart murmur (sometimes new
or changing).
• Patient may or may not have embolic phenomenon,
splenomegaly, or skin manifestations (e.g., Osler nodes,
Janeway lesions, Splinter hemorrhages).

8. LAB INVESTIGATIONS
Blood Cultures
• Minimum of three blood cultures
• Three separate venipuncture sites
• Obtain 10-20mL in adults and 0.5-5mL in children
Positive Result
• Typical organisms present in at least 2 separate samples.
• Three or a more positive blood cultures in which the first and last
samples were collected at least one hour apart.
• The most common cause of negative cultures in patients with IE is prior
antibiotic use.
CBC – Look for a normochromic normocytic anemia and/or a
leukocytosis.
ESR and CRP - Look for an elevated erythrocyte sedimentation rate
and/or an elevated C-reactive protein which are present 90-100% of the
time.

9. LAB INVESTIGATIONS(Cont)
Rheumatoid Factor - Occasionally there will be an
elevated levels of Rheumatoid Factor, particularly in
patients who have been infected for six weeks or more.
(Minor Duke’s Criteria)
UA - Urinalysis may reveal microscopic or gross
hematuria, proteinuria, and pyuria. These findings along
with a low serum complement level indicate a
glomerulonephritis or “immunologic phenomena”. (Minor
Duke’s Criteria)
• electrocardiogram,
• chest radiograph, and
• echocardiogram

10. Diagnosis of Infective EndocarditisAccording to the
Modified Duke Criteria
Major Criteria
Blood culture positive for infective endocarditis
• Typical microorganisms consistent with infective endocarditis
from two separate blood cultures:
• Viridans streptococci, Streptococcus bovis, HACEK group,
Staphylococcus aureus; or
• Community-acquired enterococci, in the absence of a primary
focus; or Microorganisms consistent with infective endocarditis
from persistently positive blood cultures, defined as follows:
• At least two positive cultures of blood samples drawn greater
than 12h apart; or
• All of three or a majority of four or more separate cultures of
blood (with first and last sample drawn at least 1 h apart)
• Single positive blood culture for Coxiella burnetii or antiphase I
immunoglobulin G antibody titer greater than 1:800

11. Diagnosis of Infective EndocarditisAccording to the
Modified Duke Criteria(Cont)
Evidence of endocardial involvement
• Echocardiogram positive for infective endocarditis
(transesophageal echocardiography recommended in patients
with prosthetic valves, rated at least “possible infective
endocarditis” by clinical criteria, or complicated infective
endocarditis [paravalvular abscess]; transthoracic
echocardiography as first test in other patients), defined as
follows:
• Oscillating intracardiac mass on valve or supporting structures,
in the path of regurgitant jets, or on implanted material in the
absence of an alternative anatomic explanation; or Abscess; or
• New partial dehiscence of prosthetic valve
• New valvular regurgitation (worsening or changing of
preexisting murmur not sufficient)

12. Diagnosis of Infective EndocarditisAccording to the
Modified Duke Criteria(Cont)
Minor Criteria
• Predisposition, predisposing heart condition or injection drug
use Fever, temperature greater than 38°C (100.4°F) Vascular
phenomena, major arterial emboli, septic pulmonary infarcts,
mycotic aneurysm, intracranial hemorrhage, conjunctival
hemorrhages, and Janeway lesions
• Immunologic phenomena: glomerulonephritis, Osler nodes,
Roth spots, and rheumatoid factor
• Microbiologic evidence: positive blood culture but does not
meet a major criterion as noted above or serologic evidence of
active infection with organism consistent with infective
endocarditis
• Echocardiographic minor criteria eliminated

13. TREATMENT
The desired outcomes for treatment and prophylaxis of infective
endocarditis are to
• Relieve the signs and symptoms of the disease.
• Decrease morbidity and mortality associated with the infection.
• Eradicate the causative organism with minimal drug exposure.
• Provide cost-effective antimicrobial therapy determined by the
likely or identified pathogen, drug susceptibilities, hepatic and
renal function, drug allergies, and anticipated drug toxicities.
• Prevent infective endocarditis from occurring or recurring in
high-risk patients with appropriate prophylactic antimicrobials.

14. NON PHARMACOLOGIC TREATMENT
• Surgery is an important adjunct in the management of
endocarditis.
• In most surgical cases, valvectomy and valve
replacement are performed to remove infected tissue and
to restore hemodynamic function.

23. Prevention of Infective Endocarditis
Consider prophylaxis against IE in patients at higher risk.
Patients at higher risk include those with the following conditions:
• Presence of prosthetic heart valve
• History of endocarditis
• Cardiac transplant recipients who develop cardiac valvulopathy
• Congenital heart disease with a high-pressure gradient lesion.
As per AHA the 3 major steps in the pathogenesis of IE that are
vulnerable to antibiotic prophylaxis are the following:
Killing of the pathogen in the bloodstream before it can adhere to
the valve.
Preventing adherence to the valve/fibrin-platelet thrombus.
Eradicating any organisms that have attached to the thrombus.

24. MONITORING PARAMETERS
• Assessment of disease signs and symptoms,
• blood cultures,
• microbiologic tests,
• serum drug concentrations, and
• other tests that evaluate organ function.

25. Thank you