management of Infective Endocarditis in adults

1. Infective Endocarditis
Dr Nzau Muange

2. Definition
• IE is Infection of the Endocardium, usually involving the Valves

3. Pathogenesis
• Valvular ulceration or perforation
• Valvular insufficiency
• Decreased tenacity of the heart valve, leading to the formation of a
luminal tumour-like bulge that may impede blood flow
• Perforation of the bulging valve which will exacerbate regurgitation

4. Pathogenesis ctd
Valvular abscesses
• An abscess located at the root of the aortic valve may compress the coronary
artery and lead to angina pectoris or myocardial infarction
• An abscess located at the proximal end of the mitral valve may spread to the
left atrial wall, atrial septum, left ventricle, or even more distally

5. Pathogenesis ctd
• Pathogens proliferating in the blood stream may result in bacteraemia
or septicaemia.
• Proliferation of pathogens may induce antibody production and lead
to immune-mediated diseases, eg polyangiitis, glomerular nephritis,
arthritis, pericarditis

6. Embolism
• Embolic events are a frequent complication related to the shedding of
cardiac vegetations
• Spread most common to the brain, spleen, lung, heart, and kidney.
• Micro-emboli may not demonstrate overt clinical symptoms and may only
be discovered at the time of autopsy.
• Large emboli can cause organ ischaemia or even necrosis.
• Infective emboli may lead to local infection with progression to abscess
formation. Alternatively, embolization can result in infective vasculitis and
angioma formation, most commonly involving the cerebral arteries,
mesenteric artery, splenic artery, coronary artery, and pulmonary artery

7. Predisposition
(i) Intra-cardiac prosthetic material (e.g. prosthetic valve, pacemaker,
implantable defibrillator, and surgical baffle/conduit)
(ii) Prior history of IE
(iii) Previous valvular or CHD
(iv) Predisposition for IE (e.g. immunocompromised state or IV drug
use)
(v) Predisposition and/or recent invasive intervention with associated
bacteraemia
(vi) Evidence of congestive heart failure

8. Predisposition
(vii) Presence of a new conduction disturbance by echocardiography
(viii) Positive blood cultures with a typical IE causative organism
(ix) Presence of vascular or immunologic abnormalities indicative of an
embolic event, including Roth spots, splinter haemorrhages, Janeway
lesions, and Osler's nodes
(x) Focal or non-specific neurological symptoms and signs that may
suggest a CNS embolic event
(xi) Evidence of pulmonary embolism/infiltration (right-sided IE)
(xii) Peripheral abscesses (renal, splenic, cerebral, and vertebral)

9. Clinical Features
• Predisposed individual
• Fever associated with chills, anorexia and weight loss
• New regurgitant heart murmur
• Embolic events of unknown origin
• Sepsis of unknown origin

10. Duke’s Diagnostic Criteria
• Gold Standard is Modified Duke’s Criteria (2000)
• Diagnosis of IE is considered definitive in the presence of
(i) two major criteria; or
(ii) one major and three minor criteria; or
(iii) five minor criteria
• Diagnosis of IE is possible in the presence of
(i) one major and one minor criteria; or
(ii) three minor criteria

11. Duke’s Criteria: Major
1. Positive Blood Culture
(a) the presence of typical microorganisms consistent with IE from two separate
blood cultures, which include Viridans streptococci, Streptococcus bovis, HACEK
group, Staphylococcus aureus, or community-acquired enterococci, in the
absence of a separate primary focus
(b) microorganisms consistent with IE from persistently positive blood cultures
(at least two positive blood cultures from blood samples drawn >12 h apart; or
all of three or a majority of ≥4 separate blood cultures, with the first and last
sample drawn at least 1 h apart)
(c) a single positive blood culture for Coxiella burnetii or IgG antibody titer >1 :
800.

12. Duke’s Criteria: Major ctd
2) Evidence of endocardial involvement by:
(a) Echocardiography positive for IE with vegetation, abscess, or new
partial dehiscence of prosthetic valve
(b) New valvular regurgitation

13. Duke’s Criteria: Minor
(i) Predisposition including history of using injected drugs
(ii) Fever (with a temperature >38°C).
(iii) Vascular phenomena (including major arterial emboli, septic
pulmonary infarcts, mycotic aneurysm, intra-cranial haemorrhages,
conjunctival haemorrhages, or Janeway lesions).
(iv) Immunologic phenomena (including glomerulonephritis, Osler's
nodes, Roth's spots, or positive rheumatoid factor).
(v) Microbiological evidence (defined as either a positive blood culture
that does not meet a major criterion or serological evidence of active
infection with an organism consistent with IE)

14. Management of IE: Assessment on Admission
• Detailed History focused on Risk Factors
• Careful Physical Examination
• Duke’s criteria
NB: Fever + New Murmur means Endocarditis until proven otherwise

15. Principles of antimicrobial therapy
(i) The application of bactericidal agents
(ii) The combination of two cooperative antimicrobial drugs
(iii) Large dosage of therapy to guarantee effective tissue concentration
(iv) Intravenous delivery of therapy
(v) Prolongation of therapy (4–6 weeks)

16. Antimicrobial Therapy ctd
• Empirical Therapy: Combine
IV Benzyl Penicillin 2 MU 4hrly+IV Gentamicin 1mg/kg 8hrly+IV
Flucloxacillin 2g 6hrly
• Change antibiotics once C&S results are out
• Duration 4 weeks

17. Surgical Management
• In general, surgical management of IE is reserved for left-sided
disease.
• Approximately 50% of left-sided IE affects the mitral valve, and about
35% affects the aortic valve. In about 15% of cases, both valves are
affected.
• Half of patients require surgery because of severe complications.
Indications for early phase surgery (during antimicrobial therapy)
include heart failure, uncontrolled infection, and prevention of
embolism

18. Complications of IE: Neurological
• Neurological events develop in 20–40% of all patients with IE
• Are mainly the consequence of vegetation embolism.
• The clinical spectrum of these complications is wide and includes
ischaemic or haemorrhagic stroke, transient ischaemic attacks, silent
cerebral embolism, symptomatic or asymptomatic infectious
aneurysm, brain abscess, meningitis, toxic encephalopathy, and
seizure

19. Complications of IE: Acute Renal Failure
• Acute renal failure is a common complication of IE which occurs in
∼30% of patients
• Causes are often multi-factorial and include:
(i) Immune complex and vasculitic glomerulonephritis
(ii) Renal infarction
(iii) Haemodynamic impairment, particularly in cases associated with
heart failure, severe sepsis, or cardiac surgery
(iv) Antibiotic toxicity, notably related to aminoglycosides, vancomycin,
and even high dose penicillin
(v) Nephrotoxicity of contrast agents used during radiologic imaging

20. Complications of IE: Rheumatic
• Musculoskeletal symptoms (e.g. arthralgia, myalgia, and back pain)
are frequent during IE, and rheumatic complications may be the first
manifestations of the disease.
• Peripheral arthritis occurs in about 14% and spondylodiscitis in 3–
15% of cases.

21. Complications of IE: Splenic
• Splenic infarction occurs in 40% cases, of which 5% of cases may
progress to splenic abscess
• Streptococcus viridans and Staphylococcus aureus are the most
frequent pathogens, and Enterococcus spp. are also causative
pathogens

22. Complications of IE: Myocarditis and
Pericardiditis
• Cardiac failure may also be due to myocarditis. Ventricular
arrhythmias can indicate myocardial involvement and imply a poor
prognosis.
• Pericarditis may be associated with an abscess, myocarditis, or
bacteraemia (often as a result of S. aureus infection). Purulent
pericarditis is a rare occurrence and may necessitate surgical
drainage. Additionally, ruptured pseudo-aneurysms or fistulae may
communicate with the pericardium, with fatal consequences.
• When infection affects the bicuspid valve or the tricuspid valve,
purulent pericarditis must be considered..

23. Prevention of IE
• Prevention is primarily aimed at disrupting the association between
bacteraemia and structural heart diseases. Bacteraemia is a
prerequisite for the occurrence of IE, and patients with structural
heart abnormalities are highly susceptible to IE if they become
bacteraemic
• To prevent and reduce the incidence of bacteraemia in patients with
structural heart disease, general measures include emphasizing the
importance of good oral hygiene and regular dental examinations, as
well as skin hygiene, so as to prevent secondary infection caused by
skin or mucosal injury. It is recommended to try to avoid traumatic
examinations and operations and to strictly follow aseptic technique
if possible.

24. Prevention of IE ctd
Antibiotic prophylaxis is recommended when a high-risk procedure is
performed in the patients with any of the following conditions:
i. Previous History of IE
ii. Valvular heart disease
iii. Congenital heart disease
iv. Hypertrophic obstructive cardiomyopathy
v. Rheumatological disorders requiring glucocorticoid or
immunosuppressive therapy
vi. Injected illicit drug users

25. Prevention of IE ctd
Choice of Antibiotic is any one of the following:
a. PO Amoxycillin 3g Stat 1 Hr Preop
b. IV Amoxycillin 1g Stat 1 Hr Preop
c. PO Clindamycin 600mg Stat 1 Hr Preop