Infective Endocarditis

  • June 2020
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Infective endocarditis Assoc.Prof.Dr.Zurkurnai Yusof USM

Who gets infective endocarditis Incidence: appr. 1.7 – 6.2 cases per 100000  patient years Rates higher  in  at risk cohorts such as iv drug  users Men > women (2:1) Incidence progressively increases with age Underlying degenerative aortic and mitral predominate esp in the West

What is the underlying pathophysiology Ulceration on the valvular endothelial surface  promotes bacterial adherence: Direct contact between blood and  subendothelial components results in  production of coagulum or small clot Local inflammation promotes cells to express  transmembrane proteins that bind fibronectin

How do patients present? Fever 90% Poor appetide and weight loss Heart murmurs 80% Vasculitic phenomenon such as splinter h’rhage,  Roth spots, and GN remain common Emboli to brain, lung, or spleen in 30% of patients Mycotic aneurysm Osler’s nodes and Janeway lesions  uncommon Atypical presentation common in elderly or  immunocompromised

Osler’s node

Purpuric lesions

How to investigate endocarditis Blood cultures 3 sets drawn one hour apart No evidence  to take at temperature peaks

Micro‐organisms responsible for native valve and prosthetic  valve endocarditis in recent European survey

What to do when the cultures are negative Blood cultures negative in 14%, delaying diagnosis  and the start of treatment Commonly related to previous antibiotics  administration Fastidiuos pathogens: Legionella, Coxiella, the  HACEK gp(Haemophilus sp., Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae) Fungi: Candida, Histoplasma, and Aspergillus sp.

What to do when the cultures are negative Serological testing‐ possibility of Coxiella burnetti and Bartonella infection Histological techniques Polymerase chain reaction, to detect fastidious  and non‐culturable agents

Echocardiography Transthoracic Transesophageal Ix potential Cx:  mechanism of significant  valvular regurg perivalvular abscesses

Diagnostic criteria Von Ryen criteria: published in early 1980’s Duke criteria: 1990s Modified Duke criteria: in the latest guidelines  from ESC

Modified Duke criteria Pathological criteria Positive histology or microbiology of pathological material obtained at  autopsy or cardiac surgery Major criteria Two positive blood cultures showing typical organisms consistent with  infective endocarditis, such as Streptococcus viridans and the HACEK  group OR Persistent bacteraemia from 2 blood cultures taken > 12 hours apart or 3  or more positive blood cultures where the pathogen is less specific, such  as Staphylococcus aureus and Stap epidermidis OR Positive serology for Coxiella burnetti, Bartonella species, or Chlamydia  psittaci OR Positive molecular assays for specific gene targets

Antimicrobial treatment Choice and length of treatment dictated by pathogen isolated from cultures require collaboration of microbiologist and physician Factors to consider for empirical treatment: patient related risk factors local bacterial resistance pattern Switch to appropriate antibiotic as soon as cultures and sensitivites are  available Treatment duration: 4 to 6 weeks

Special subgroups Prosthetic valves Incidence: 0.1 to 2.3% per year 10‐15% of the cases TOE almost always indicated Classifications: Early Late Early onset:  Staphylococci predominate Late onset: mirrors that of native valve endocarditis Complications: common aortic root abscess

Special subgroups Prosthetic valves Treatment:  difficult prolonged antibiotics surgery when needed, is technically demanding Overall mortality: 40‐50% Specialist care mandatory

Special subgroups Intravenous drug users Incidence: 1‐5% a year rising in UK Equal frequency on right sided and left sided Most common pathogen: Staph aureus Problems: Management difficulties recurrence high cardiac surgeons reluctancy to operate mortality high

Who needs surgery Surgery‐ potentially life saving Outcome related to: valvular regurgitation abscess formation heart failure embolic complications Rarely vegetations cause valve obstruction Overall, surgery is needed in appr. 50% of the cases Careful timing essential for good outcome

Who needs surgery Urgent surgery should be considered: Haemodynamic compromise due to valve destruction Persistent fever despite appropriate antibiotic treatment Development of abscesses or fistulae due to perivalvular spread of  infection Involvement of highly resistant organisms PVE (particularly in the early postoperative phase) Large vegetations with high embolic potential (> 10 mm or on the mitral valve

Prophylaxis

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