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Objectives :
Infective Endocarditis
★ Understand Infective Endocarditis definition
★ Pathophysiology of endocarditis
★ Diagnostic criteria of infective endocarditis
★ Recognize the risk factors, signs, and symptoms
of infectious endocarditis.
★ Anticipate possible complications of infective
endocarditis
★ Treatment of endocarditis and appreciation of the
necessity of rapid treatment.
★ Endocarditis prophylaxis
Original text Females slides Males slides Doctor’s notes 438 Doctor’s notes 439 Text book Important Golden notes Extra
Editing file
Color index
Introduction to IE^2
◄ What’s Infective Endocarditis (IE)? اﻟﺗﮭﺎب اﻟﺷﻐﺎف اﻟﻌدواﺋﻲ ● Infective Endocarditis (one of the diseases called great mimicker) is an infection of the endocardial surface of the heart, which may include; one or more heart valves^1 (native or prosthetic), Chordae tendineae , a septal defect (e.g. ASD, VSD), AV shunt, Mural endocardium. (IE can extend to all layers of the heart). leading to formation of bulky friable vegetations composed of thrombotic debris and organisms. (fibrin, RBCs and inflammatory cells) ● IE develops most commonly on the mitral valve, followed by the aortic valve, combined mitral & aortic valve, tricuspid valve (especially In IVDU) & rarely, the pulmonic valve.
◄ Pathogenesis of IE
Endothelial damage Caused by turbulent blood flow produced by either a congenital or acquired heart disease (congenital abnormalities of cardiac valves, prosthetic valves). This flow can be from a high to a low pressure chamber^3 , High velocity jet or across a narrowed orifice (e.g. Aortic stenosis, Mitral stenosis) which traumatizes the endothelium.
01 02 03
Formation of NBTE Endothelial damage creates a predisposition for deposition of platelets and fibrin on the surface of the endothelium, which results in Nonbacterial Thrombotic Endocarditis (NBTE)^4.
Bacterial or fungal adherence Invasion of the bloodstream (via mouth, skin or intravenous lines, or gastrointestinal tracts) by a microbial species that has the pathogenic potential to colonize this site (endocardium). This will result in the proliferation of bacteria within NBTE (leading to infiltration by neutrophils and macrophages) forming vegetations^5 (hallmark of IE)
What’s the source of the bacteremia in IE? Trauma to a mucosal surface heavily populated by endogenous microflora; Such as the gingiva around the teeth and oropharynx (Old: GI tract, urethra and vagina). This will releases many different microbial species transiently into the bloodstream which will leads to transient bacteremia^6 caused by organisms e.g. Viridans group streptococci.
◄ Epidemiology of IE
● Developing countries (endemic RF), Subacute course, viridans group streptococci. ● Developed countries, acute illness, Staphylococcus aureus(etiology is different from country to country, in north american countries drug abuse is very common, thus IE is usually caused by staph, in saudi the most common cause is streptococcus viridans), with numerous anatomic sites of metastatic foci of infection and worse outcomes. ● Mechanical prosthetic & bioprosthetic valves exhibit equal rates of infection. ● More common in males (because of drug abuse) ● It occurs in 5-7 per 100,000 person-years before 2000 and now 15 per 100,000 persons-years^2. ● It remains a life threatening disease with significant mortality (About 20%) and morbidity.
● The IE is the net result of the complex interaction between the bloodstream pathogen with matrix molecules and platelets at sites of Endocardial cells damage.
1-Because its Avascular parts of the heart and its an area where leukocytes doesn't go to. 2- Why is it increased nowadays? Because of the increase in IVDU. 3-Like in Ventricular septal defect; the left side of the heart has higher pressure than the right, so there will be turbulent blood flow from Lt to Rt traumatizing the endothelium. 4- AKA Marantic Endocarditis, it’s associated with metastatic cancer (Has poor prognosis), It becomes IE when bacterial colonization occurs. Another form of Nonbacterial endocarditis (NBE) is Libman - Sacks Endocarditis, which typically occurs in individuals with SLE. Other causes of NBE include: Cancer of lungs, ovaries. 5- (1) Local destruction: Vegetations may destroy the valve itself which may lead to regurgitation, HF etc, It also may form perivalvular abscess if it’s in aortic valve (Dangerous and Surgery is required in this case). (2) Septic embolization: Vegetations may detach → Septic embolization to any part of the body e.g. Peripherally, spleen, liver, lung, eyes , brain (mycotic aneurysm). Septic embolization may lead to stroke, abscess formation, Gangrene, Hematuria (→ Anemia) and elevated ESR, septic arthritis. Vegetations may also cause(3) immunological reaction → Glomerulonephritis, arthritis, Rheumatoid factor, Antinuclear antibody, CRP and ESR. 6-Clinically what symptoms and sign will appear in bacteremia : chills - Rigors - Fever.
Classification of IE
◄ Acute vs Subacute IE
Acute Subacute
Causative organism
Staphylococcus aureus (High virulence organism)
Strept. viridans or bovis (Low virulence organisms)
Site
Normal heart valves (Most commonly Tricuspid) Previously damaged heart valves
Prognosis If untreated, fatal in less than 6 weeks
If untreated, takes much longer than 6 weeks to cause death
◄ Overview on causative organisms
1- What carries more risk of IE, native or prosthetic valve? Prosthetic bc it’s metal so has no blood supply → no abx can reach it 2- nosocomial infections in recently discharged patients
Staph aureus (Including MRSA^2 )
● Aggressive acute IE. Metastatic infection, valve destruction. ● Mortality 25-40% (left heart)
Coagulase negative Staph e.g. staph epidermidis
● Foreign body infection/prosthesis ● Nosocomial infection
Strep. gallolyticus (previously known as Strep. bovis) And Clostridium Septicum
● GI flora associated with polyps and colon cancer (do Colonoscopy) ● Subacute endocarditis, Highly sensitive to penicillin.
Beta-hemolytic strept group A-B-C-G ● Frequent intracardiac & extracardiac complications, abscesses
Enterococci (faecalis, Faecium) ● GI flora, associated with UTI/ nosocomial infection
What’s the most common overall causative agent? Streptococcus viridans ● Patient with history of VHD (e.g. Chronic rheumatic heart disease and MVP) and dental procedure → Streptococcus viridans ● IV drug user presented with endocarditis → Staphylococcus aureus ● Patient who has done prosthetic valve surgery, presented with endocarditis later → Staphylococcus epidermidis or aureus (If within 60d of surgery) or Streptococcus viridans (If after 60d of surgery) ● Patient has colorectal cancer and presented with endocarditis → Streptococcus bovis, clostridium septicum ● Patient presented with endocarditis but all blood cultures are negative → HACEK (Coxiella and Bartonella)
(Usually an exam Q)
Nature of the valve involved/ Type of lesion^1
Onset and progression
Acquisition of the infection
Native
Prosthetic
Acute (Symptoms up to 6wks)
Subacute (Symptoms up to 6wks-3m)
Nosocomial
Community
Early Late^ IV drug abuse
Congenital
Chronic (Symptoms -3months)
Microbiology of IE
◄ How to determine the causative agent?
● It vary depending on the population:
- IV drug abusers
- Patients with Prosthetic Heart Valve (PHV)
- Hospital acquired vs Community acquired
● What are the most common causative organisms of IE worldwide?
- Streptococci: ○ Common cause of community acquired IE
- Staphylococci:
○ Most common cause in the US & most developed countries.
○ Health care-associated IE
- Enterococci
1- e.g. Enterococcus faecalis, and Strep. gallolyticus (previously known as Strep. bovis), they enter blood through bowel and Urinary tract. Patients who are found to have endocarditis caused by Strep. gallolyticus should undergo colonoscopy, since this organism is associated with colon cancer. 2- In females slides it’s 12 months, according to the female Dr, 60 days is the old classification, the new one is 12 months. (In Males slides and Kumar it’s 60d) 3- Culture-negative endocarditis usually is caused by prior administration of antibiotics before obtaining blood cultures or by infection with fungi or fastidious organisms. 4- In Q fever endocarditis due to Coxiella burnetii, the patient often has a history of contact with farm animals. The aortic valve is usually affected and there may also be hepatitis, pneumonia and purpura.
Click here for a few pics present in females slides only
Native valve IE IV drug abusers IE Prosthetic valve IE
- Streptococci: (50-70%) a. Streptococcus viridans (50%) (in mitral valve prolapse, recent dental extraction)
- Staphylococci: (~25%) a. Mostly Coagulase +ve Staph aureus Or Staph. Epidermidis
- Enterococci^1 ( ~10%)
- HACEK: ● Haemophilus species, Actinobacillus, Actinomycetemcomitans, Cardiobacterium hominis, Eikenella, Kingella
○ Skin is the most predominant source of infection. ○ 70 - 100% of Right sided IE results in pneumonia and septic emboli. ○ It commonly affects tricuspid valve.
A) Early onset: (< 60d^2 after surgery)
It usually reflects perioperative contamination with Incidence around 1%.
- Staph. Epidermidis (30%) or Staph. Aureus (20%).
- Gram -ve aerobes (20%)
- Fungi (10%)
- Strep and Entero (5-10%)
B) Late onset: (>60d^2 after surgery)
Occurs after endothelialization with of Incidence 0.2 -0.5 %، due to transient bacteraemia from dental, GI or GU.
- Streptococcus viridans (resemble native valve IE)
Culture negative endocarditis^3 (Female slides only)
- HACEK: Fastidious gram-negative bacilli, Positive blood culture after 5 days of incubation & maybe longer, large vegetations. (culture -ve species, if you suspect IE but the culture is -ve, you have to think of HACEK) (identification of HACEK is difficult because conventional culture methods produce inconclusive results in cases of fastidious and slow-growing organisms)
- Coxiella burnetii (Q fever):^4 Subacute endocarditis, elevated IgG
- Bartonella: Cat scratch disease
- Fungi (candida): risk factors are immunosuppression, prosthesis, central line, IVDU, invasive endocarditis
- Others: Brucella (history of contact with goats or cattle), tropheryma whipplei, Mycoplasma, legionella
- Staphylococcus aureus 60%
- Streptococci and Enterococci (20%)
- Gram -ve bacilli (10%)
- Fungi (Candida and Aspergillus) (5%).
Diagnostic criteria of IE
◄ Duke criteria
Major criteria
- Positive blood culture:
a) Typical organism from two separate cultures e.g. Strep, Staph, HACEK
b) Persistent positive blood cultures
i) ≥ 2 positive blood cultures of blood samples drawn >12 hrs apart
ii) All of 3 or a majority of ≥ 4 separate cultures of blood (with 1st and last samples drawn ≥ 1h
apart)
c) Single positive culture for coxiella burnetii or phase I IgG antibody titre > 1:
- Endocardial involvement: (Check definitions next page)
a) Positive echocardiographic findings of vegetations, Abscess , pseudoaneurysm
,intracardiac fistula , valvular perforation, aneurysm or New partial
dehiscence(unstable/detached)of prosthetic valve
b) Abnormal activity around the site of prosthetic valve implantation detected by F-FDG
PET/CT (only if the prosthesis was implanted for >3 months) or radiolabeled leukocytes
SPECT/CT.
c) Definite paravalvular lesion by cardiac CT
d) New valvular regurgitation
Minor criteria
- Fever: > 38oC
- Echo findings: Any finding not involved in the major criteria e.g. calcification
- Vascular phenomena (Including these detected only by imaging):
a) Major arterial emboli , septic pulmonary infarcts , infectious (mycotic) aneurysm ,
intracranial hemorrhage , conjunctival hemorrhage and janeway’s lesions.
- Evidence from microbiology:
a) Positive blood culture but does not meet a major criterion as noted above or serological
evidence of active infection with organism consistent with IE.
- Risk factors and predisposition:
a) Such as heart conditions (e.g. VHD, prosthetic valve, previous IE) or IV drug users
- Immunological phenomena:
a) Glomerulonephritis , osler’s nodes , Roth’s spots and Rheumatoid factor
(Usually an exam Q) BE FEVER I
Diagnostic criteria of IE cont’
◄ Duke criteria
● Definitive IE: (Begin treatment right away) ○ Clinical criteria: Patients with 2 major, OR 1 major and 3 minor, OR 5 minor. ○ Pathologic criteria: Microorganisms or pathologic lesions: demonstrated by culture or histology in a vegetation, or in a vegetation that has embolized, or in an intracardiac abscess ● Possible IE: (Requires further tests) ○ Clinical criteria: Patients with 1 major and 1 minor, OR 3 minor. ● Rejected IE: ○ Firm alternate Diagnosis for manifestation of IE ○ Resolution of manifestations of IE, with antibiotic therapy for ≤ 4 days ○ No pathologic evidence of IE at surgery or autopsy, after antibiotic therapy for ≤ 4 days)
◄ Anatomic and echographic definitions
Pathology Surgery/necropsy Echocardiography
Vegetation
Infected mass attached to an endocardial structure or an implanted intracardiac material
Oscillating or non-oscillating intracardiac mass on valve or other endocardial structures, or on implanted intracardiac material
Abscess
Perivalvular cavity with necrosis and purulent material not communicating with the cardiovascular lumen
Thickened, non-homogeneous perivalvular area with echodense or echolucent appearance
Pseudoaneurysm
Perivalvular cavity communicating with the cardiovascular lumen
Pulsatile perivalvular echo-free space, with colour doppler flow detected
Perforation
Interruption of endocardial tissue continuity
Interruption of endocardial tissue continuity traversed by colour doppler flow
Fistula
Communication between 2 neighbouring cavities through a perforation
Colour-doppler communication between two neighbouring cavities through a perforation
Valve aneurysm Saccular outpouching of valvular tissue
Saccular bilging of valvular tissue
Dehiscence of a prosthetic valve
Dehiscence of the prosthesis Paravalvular regurgitation identified by TEE/TOE, with or without rocking motion of the prosthesis
Complications of IE
◄ Complications of IE
Embolic
Risk factors for embolic (Females slides only)
● Size of vegetation (>10 mm) ● Left side vegetations ● Staph. Aureus ● Fungal pathogens Uncommon after 2 weeks of effective treatment
Complications
● Neurological manifestations (1⁄3 of cases): caused by
stroke either due to major embolism to MCA (25%) or ICH from a ruptured mycotic aneurysm (2-10%) or hemorrhagic transformation of stroke. ● MI, PE (Septic emboli “Pulmonary cavitation”) ● Ischemic limb, Mesenteric ischemia ● Splenic or renal infarction ● Digital infarcts
Local spread
● Congestive Heart failure (The commonest complication):
Caused by extensive valvular destruction, ruptured chordae tendineae, fistulas, valve obstruction, Myocarditis, Coronary artery embolism, MI and Myocardial Abscesses
● Paravalvular abscess: Most common in aortic valve^1
, IVDA, staph, aureus ● AV block / conduction disorders: Myocardial abscesses ● Pericarditis
Metastatic spread
● Rt. Sided vegetations: Lung abscesses, Pyothorax /
Pyo-pneumothorax
● Lt. Sided vegetations: Pyogenic Meningitis, Splenic
Abscesses, Pyelonephritis, Osteomyelitis ● Metastatic abscesses ● Septic arthritis
Formation of immune complexes
● Immune complex glomerulonephritis leading to Acute renal failure ● Immunologic arthritis
Why would fever persist for a long time? (Females slides only) Resolution of fever occurs in 5-7 days; persistence of fever indicates: ● Abscess ● Infected indwelling catheters or devices ● Septic embolization ● An extracardiac site of infection (native or prosthetic) ● Inadequate antibiotic treatment of resistant organism ● An adverse reaction to the antibiotic therapy itself (uncommon)
Septic Emboli
1- monitored by an ECG “prolonged PR interval due to the close proximity between AV node and root of aortic valve”
Management of IE
◄ Medical therapy (Antibiotics)
● Empirical therapy: Empirical treatment depends on the mode of presentation, the suspected organism and the presence of a prosthetic valve or penicillin allergy.
● After identification of the causal organism: Principles of medical therapy: Treat vegetations with with high dose of IV bactericidal abx for prolonged duration (Generally native valve → 2-4wks and Prosthetic valve → 6-8wks.)
◄ Surgical therapy
● Indications for cardiac surgery in IE: A. Heart failure due to valve damage e.g. Dehiscence, intracardiac fistula or prosthetic dysfunction B. Failure of abx therapy: persistent infection (bacteremia or fever) lasting >5-7 days after starting abx C. Large/persistent vegetations on left-sided heart valves with echo appearance suggesting high risk of recurrent emboli. D. IE complicated by heart block, annular abscess, or destructive perforating lesions. E. Patients with fungal endocarditis often require cardiac surgery. F. Prosthetic valve IE caused by fungi or highly resistant organisms.
Acute onset Subacute onset^2 Prosthetic valve IE
Blood culture and start treatment within 3 hours. Abx: Vancomycin and Gentamicin
Blood culture then antibiotic can be started within 3d Abx: Amoxicillin with/without gentamicin
Abx: Vancomycin, gentamicin and rifampicin
Staphylococcus Strep. viridans or bovis
Native valve
● MSSA: Flucloxacillin OR Naficillin OR
Oxacillin for 4wks
● MRSA & Penicillin allergic Pts:
Vancomycin for 4-6wks
Prosthetic valve
● MSSA: Flucloxacillinwith gentamicin
and rifampicin
● MRSA & Penicillin allergic Pts:
Vancomycin,with gentamicin and rifampicin
Penicillin susceptible:
● IV Ceftriaxone once daily for 4 weeks (cure rate
98%) ● OR Ceftriaxone 2g for 2 weeks followed by oral amoxicillin for 2 weeks ● OR IV penicillin G OR IV amoxicillin for 4 weeks ● In B-lactam allergic patients: Vancomycin.
Penicillin resistant:
● Ceftriaxone with Gentamicin OR Penicillin G OR Amoxicillin. ● In B-lactam allergic patients: Vancomycinwith Gentamicin
1-Exam Q : What is the main state for treatment = Antibiotics. (usually you start broad then you narrow down based on the culture). 2- If the presentation is subacute, antibiotic treatment should ideally be withheld until the results of blood cultures are available. However, if empirical antibiotic treatment is considered necessary give the ones mentioned.
Click here for a few treatment tables present in females slides only
Enterococci: Ampicillin and gentamicin & for HACEK group use Ceftriaxone Feel lost? click here
Summary
Infective endocarditis
Definition An infection of the endocardial surface of the heart, which may include; one or more heart valves (native or prosthetic), the mural endocardium
Pathophysiology Endothelial damage^ →^ NBTE formation^ →^ Bacterial adherence^ →^ Formation of vegetations (Hallmark of IE)
Risk factors Poor dentition, Cardiac issues (e.g. Congenital heart disease, VHD , prosthetic valve), IVDU.
Onset
Acute Subacute
● Causative organism: Staph. aureus ● Site: Normal valves ● Prognosis: If untreated, fatal in < 6 weeks
● Causative organism: Strep. viridans ● Site: Previously damaged valves ● Prognosis: If untreated, takes > 6 weeks to cause death
Microbiology of IE
What’s the most common overall causative agent? Streptococcus viridans ● Patient with history of VHD (e.g. Chronic rheumatic heart disease and MVP) and dental procedure → Streptococcus viridans ● IV drug user presented with endocarditis → Staphylococcus aureus ● Patient who has done prosthetic valve surgery, presented with endocarditis later → Staphylococcus epidermidis or aureus (If within 60d of surgery) or Streptococcus viridans (If after 60d of surgery) ● Patient has colorectal cancer and presented with endocarditis → Streptococcus bovis ● Patient presented with endocarditis but all blood cultures are negative → HACEK ( Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
S & S FROM JANE
Duke criteria
BE FEVER I Definitive IE: Clinical criteria: Patients with 2 major, or 1 major and 3 minor, or 5 minor Possible IE: Clinical criteria: Patients with 1 major and 1 minor, or 3 minor
Investigations
● Blood cultures ● Echocardiography: TTE should be attempted first. TEE should be used if TTE is nondiagnostic ● Others: ECG, CBC, RFT, Inflammatory markers, CXR
Complications Focal neurologic deficits from embolic strokes, splenic abscess, Congestive heart failure caused by valvular insufficiency, and glomerulonephritis.
Treatment
Staphylococcus Strep. viridans or bovis
Native valve ● MSSA: Flucloxacillin ● MRSA & Penicillin allergic Pts: Vancomycin Prosthetic valve ● MSSA: Flucloxacillinwith gentamicin and rifampicin ● MRSA & Penicillin allergic Pts: Vancomycin, with gentamicin and rifampicin
Penicillin susceptible: ● IV Ceftriaxone once daily (third generation cephalosporin) OR IV penicillin G OR IV amoxicillin for 4 weeks ; OR Ceftriaxone 2g for 2 weeks followed by oral amoxicillin for 2 weeks. ● In B-lactam allergic patients: Vancomycin. Penicillin resistant: ● Ceftriaxone with Gentamicin OR Penicillin G OR Amoxicillin. ● In B-lactam allergic patients: Vancomycinwith Gentamicin
EXTRA Helpful figures
GOOD LUCK!
Edited by 439 Medicine team:
This work was originally done by 438 Medicine team:
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- Raghad AlKhashan
- Amirah Aldakhilallah
- Mashal AbaAlkhail
- Ibrahim AlAsous
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Member : Ahmed Alhawamdeh
Note taker : Norah Alsalem
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