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Infective endocarditis

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Infective endocarditis
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Infective endocarditis

  2. 2. INTRODUCTION 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. It may be caused usually by a bacterium, but may also involves a rickettsia, chlamydia or fungus. Its intracardiac effects include severe valvular insufficiency, which may lead to intractable congestive heart failure, and myocardial abscesses.
  3. 3. THE PROTOTYPE LESION The vegetation • Variable in size • Amorphous mass of fibrin & platelets • Abundant organisms • Moderate inflammatory cells
  4. 4. Predisposing Factors Rheumatic Heart Disease • 7 – 18% of cases in recent reported series • • Mitral site more common in women • • Aortic site more common in men Congenital Heart Disease • • 10 – 20% of cases in young adults • • 8% of cases in older adults • • PDA, VSD,TOF, Bicuspid Aortic Valve (esp. in men>60) Intravenous Drug Abuse • – Risk is 2 – 5% per pt./year • – Tendency to involve right-sided valves Distribution in clinical series • – 46 – 78% tricuspid • – 24 – 32% mitral • – 8 – 19% aortic • – Underlying valve normal in 75 – 93% • – S. aureus predominant organism
  5. 5. Implantable pacemakers and cardioverter defibrillators • They are infected within a few months of implantation • – Generator pocket (most common) • – Proximal leads • – Portion of leads in direct contact with endocardium, is the most challenging to treat. • Of pacemaker infections, 75% are produced by staphylococci. Degenerative valve disease • Myxomatous mitral valve • Hypertrophic cardiomyopathy • Degenerative calcific valvular stenosis • Valvular damage from surgery, autoimmune conditions or old age.
  6. 6. CLASSIFICATION Classified according to the temporal evolution of disease, the site of infection, the cause of infection, or the predisposing risk factor. • Acute (short incubation) vs. subacute (long incubation) • Culture-positive vs. culture-negative • Right sided vs. left sided • Nosocomial vs. community-acquired • Native-valve endocarditis vs. prosthetic-valve
  7. 7. Acute and Subacute Bacterial Endocarditis Acute • Affects normal heart valves • Rapidly destructive • Metastatic foci • Commonly Staph. aureus • If not treated, usually fatal within 6 weeks Subacute Often affects damaged heart valves • Indolent nature • Most commonly Strepto. viridans or Enterococcus • If not treated, usually fatal by one year
  8. 8. Native Valve Endocarditis 1.Community acquired NVE: • Among 25-35% of total cases of NVE ,45% belongs to community acquired endocarditis. • Most common organisms includes: Streptococci>staph aureus>culture negative>CONS. 2.Health care associated NVE: • 55% of total NVE cases belongs to this group. • Most common organisms includes: Staph aures(MRSA)>Enterococci>streptocooci>CONS
  9. 9. Prosthetic Valve Endocarditis • PVE accounts for 16-30% of cases of IE. • The valves in the mitral valve position are more susceptible than those in the aortic areas Early PVE occurs within 60 days of valve implantation • – usually due to intraoperative contamination or a postoperative bacterial contamination which is usually nosocomial in nature. • – staph aureus , coagulase-negative staphylococci, gram-negative bacilli, and Candida species most common. Late PVE occurs 60 days or more after valve implantation • – Late prosthetic valve endocarditis is usually due to community acquired microorganisms • – Staphylococci, alpha-hemolytic streptococci, CONS and enterococci are the common causative organisms
  10. 10. MICROBIOLOGY IN NUT SHELL The oral cavity, skin, and upper respiratory tract are the respective primary portals Streptococci • – Alpha-haemolytic Streptococci (viridans – S. mitis, S. oralis) 30-40% (subacute) • – Enterococci (E. faecalis) 5-18% (subacute) • – Beta-haemolytic streptococci (e.g. Gp A Strep) – rare (acute) Staphylococci • – S. aureus 10-27% (acute) • – Coagulase negative staphylococci (Staph epidermidis) :1-3 % (mainly prosthetic valve risk, subacute) Fungi • – Candida – IVDU at risk (usually indolent) • – Aspergillus – rare Gram-negative bacteria – rare Culture-negative endocarditis :HACEK, Q-fever – cases do occur, subacute
  11. 11. Culture-negative endocarditis can be due to: • Micro-organisms that require a longer period of time to be identified in the laboratory • Prior antibiotic treatment. Fungal endocarditis • HACEK Group (gram neg.coccobacilli.) • • Haemophilus spp. • • Aggregatibacter species • • Cardiobacterium hominis • • Eikenella corrodens • • Kingella kingae • Coxiella burnetii - Q fever endocarditis • –farm animals • –hepatic complications and purpura • –Life-long antibiotic therapy may be required • Brucella species, Chlamydia species: • h/o contact with goats or cattle • –often affects the aortic valve
  12. 12. ETIOLOGY
  13. 13. PATHOPHYSIOLOGY Modes of endothelial injury NonbacterialThrombotic Endocarditis(NBTE) Bacteraemia… • High velocity jet • Flow from high pressure to low pressure chamber • Flow across narrow orifice of high velocity • Endothelial injury • Hypercoagulable state • Platelet-fibrin thrombi • delivers organisms to the damaged (sticky)endocardial surface • adherence & colonisation of NBT infected vegetation
  15. 15. Marantic Endocarditis • NBTE due to hypercoagulable state- Malignancy, chronic diseases, SLE, APLA • Uninfected vegetation seen.
  16. 16. Clinical manifestation • Cytokine production—arise from damage to intracardiac structures; • Embolization of vegetation fragments, leading to infection or infarction of remote tissues; • Hematogenous infection of sites during bacteremia; • Tissue injury due to the deposition of circulating immune complexes or immune responses to deposited bacterial antigens
  17. 17. Cardiac Manifestations  New regurgitant murmurs- Approx.85% of cases.  CHF- 30 to 40%- due to valvular damage (aortic>mitral), myocarditis, intracardiac fistula  Perivalvular abscess Fistulae (Root of aorta to chambers/ between cardiac chambers) Pericarditis  Heart block/ MI due to embolic phenomena
  18. 18. Noncardiac Manifestations Nonspecific signs – • Petechiae, • Subungal or “splinter” hemorrhages, • Clubbing, Splenomegaly • Osler’s Nodes, • Janeway lesions, and Roth Spots Embolic phenomena include systemic, cerebral and pulmonary emboli are common in >50 % cases. Hematogenous seeded focal infection occurs most often in the skin, spleen, kidneys, skeletal system, and meninges.
  19. 19. Petechiae • Common (40-50%) but nonspecific finding • Seen on palpebral conjunctivae, the dorsa of the hands and feet, the anterior chest and abdominal walls, the oral mucosa, and the soft palate • Result from local vasculitis or emboli
  20. 20. Subungual (splinter) hemorrhages • 1. Nonspecific,Nonblanching (10%) • 2. Usually 2-3mm long in long axis of nail • 3. Initially blue-purple in colour,change to brown of black in 1-2 days • 4. Move distal with nail growth
  21. 21. Janeway Lesions • 1. More specific • 2. Erythematous, blanching macules • 3. Nonpainful • 4. Located on palms and soles • 5. Micro abscesses of the dermis with marked necrosis and inflammatory infiltrate not involving the epidermis, • Due to the deposition of circulating immune complexes in small blood vessels
  22. 22. Osler’s Nodes • More specific • Painful and erythematous nodules • Located on pulp of fingers and toes • More common in subacute IE • Due to infective emboli or immune complex deposits • 4 P’s: Pink Painful Pea-sized Pulp of the fingers/toes
  23. 23. Roth Spots Eye • Roth's spots are retinal hemorrhages flame shaped with white or pale centers composed of coagulated fibrin. • Observed via fundoscopy or slit lamp examination
  24. 24.  Signs of neurologic disease occur in as many as 40% of patients due to embolic stroke with focal neurologic deficits, seizures, intracerebral hemorrhage and multiple microabscesses.  Signs of pulmonary and systemic septic emboli more common with tricuspid endocarditis  Signs of congestive heart failure, such as distended neck veins  Splenomegaly (splenic rub d/t splenic infarction)  Risk for emboli is increased when vegetation >1cm asso.with infection involving
  25. 25. Blood cultures • Blood cultures remain a cornerstone of the diagnosis of IE cases and should be taken prior to starting treatment in all case. during the prior 2 weeks • Sampling of intravascular lines should be avoided . • As per AHA and ESC - At least three sets of blood cultures collected from different venipuncture sites, with at least 1 h between the first and last draw. • As per BSAC- Collection of two sets of blood cultures within 1 h of each other in patients with suspected endocarditis and acute sepsis and three sets of blood cultures spaced from one another by at least 2 h, should be obtained from different venipuncture sites over 24 h in cases of suspected subacute or chronic endocarditis.
  26. 26. Three sets of blood cultures, with each set including one aerobic and one anaerobic bottle, are collected.  Alternatively, two sets may be collected, with two aerobic and one anaerobic bottle per set (i.e., a total of six blood culture bottles) 10-20 ml of blood per Bactec or BacT/Alert bottle) being essential. As per study done by M. Liesman Et al,2019 published in journal o f clinical microbiology - routinely spacing blood culture draws in cases of suspected endocarditis not recommended. There is no difference in yield if blood is collected simultaneously or several hours apart. (CMDT 2019)
  27. 27. Culture Negative” IE (5-10%) • Infective endocarditis may be culture negative either due to prior antibiotic treatment or due to atypical microbial organisms or due to fungus etc non bacterial endocarditis. • Less common with improved blood culture methods • Special media required - Brucella, Mycoplasma, Chlamydia, Histoplasma, Legionella, Bartonella • Longer incubation may be required  HACEK • Coxiella burnetii (Q Fever), Trophyrema whipplei will not grow in cell-free media
  28. 28. Non-Blood-Culture Tests 1. Serologic tests---- Brucella, Bartonella, Legionella, Chlamydia psittaci, and C. burnetii. 2. vegetations recovered at surgery or by embolectomy- • culture; • special stains; • polymerase chain reaction (PCR) recovery of microbial DNA or DNA encoding the 16S or 28S ribosomal unit (16S rRNA or 28S rRNA)
  29. 29. Cardiac Imaging - Echocardiography Transthoracic echocardiography (TTE) – First line if suspected IE – Native valves Trans Esophageal echocardiography (TEE) – Prosthetic valves – Intracardiac complications – Inadequate TTE – Fungal or S. aureus or bacteremia
  30. 30. Modified Duke Criteria Definite IE • Microorganism (via culture or histology) in a valvular vegetation, embolized vegetation, or intracardiac abscess • Histologic evidence of vegetation or intracardiac abscess Possible IE • – 2 major • – 1 major and 3 minor • – 5 minor Rejected IE • Resolution of illness with four days or less of antibiotics • presence of a firm alternative diagnosis • No histological evidence of endocarditis are seen
  31. 31. Differential Diagnosis(SBE Mimickers) • Antiphospholipid syndrome • • Primary cardiac neoplasms---atrial myxoma • • Marantic Endocarditis(NBTE) • • Systemic lupus erythematosus • • Reactive arthritis
  32. 32. Treatment Case fatality is approximately 20% and even higher • –those with prosthetic valve endocarditis • –infected with antibiotic resistant The major goals of therapy for infective endocarditis (IE) are to • – eradicate the infectious agent from the thrombus • – address the complications of valvular infection. Parenteral (IV) antibiotics • – High serum concentrations to penetrate avascular vegetation’s. • – Prolonged treatment to kill dormant bacteria clustered in vegetation’s
  33. 33. • Modify empiric therapy once cultures/sensitivities known • Long duration 4-6 weeks Rx is required Empirical treatment depends • •on the mode of presentation, • •suspected organism • •whether the patient has a prosthetic valve Acute: flucloxacillin and gentamicin Subacute or indolent presentation: benzyl penicillin and gentamicin Penicillin allergy, PVE or suspected methicillin-resistant Staph. aureus (MRSA) infection: triple therapy with vancomycin, gentamicin and oral rifampicin
  34. 34. Antibiotic Therapy Effective antimicrobial treatment should • lead to defervescence within 7 – 10 days Persistent fever in: • IE due to staph, pseudomonas, culture negative • IE with paravalvular abscess, extracardiac abscesses (spleen, kidney), or complications (embolic events) • Drug reaction or complications of hospitalization
  35. 35. ANTITHROMBOTIC THERAPY • There is no indication for the initiation of antithrombotic drugs (thrombolytic drugs, anticoagulant or antiplatelet therapy) during the active phase of it dose not reduces the risk of emboli in patients with NVE • In patients already taking oral anticoagulants, There is a risk of intracranial haemorrhage which seems to be highest in patients with S. aureus
  36. 36. Cardiovascular Implantable Electronic Device (CIED) Endocarditis • Most common microorganisms involve: staph aureus > CONS • Most Common Site : GENERATOR POCKET>LEADS • Complete device and lead removal in definite CIED infection, as evidenced by valvular and/or lead endocarditis or sepsis. • Generator pocket infection without bacteremia is treated with a 10- to 14-day course, some of which can be given orally
  38. 38. Antibiotic Prophylaxis Recommended only in manipulation of gingival tissue or the periapical region of the teeth or perforation of the oral mucosa (including surgery on the respiratory tract) Not advised for gastrointestinal or genitourinary tract procedures.
  39. 39. What to give ?
  40. 40. COMPLICATIONS OF ENDOCARDITIS Systemic emboli • –Risk depends on valve (mitral>aortic), size of vegetation, (high risk if >10 mm) • Splenic abscess—3-5% • Mycotic aneurysms 2-15%--- headaches, focal neurologic symptoms, or hemorrhage ,encephalitis • Vertebral osteomyelitis, Septic arthritis • Hypoxia from pulmonary emboli Cardiac • –congestive cardiac failure-valvular damage, • –more common with aortic valve endocarditis, • –higher mortality, • –need for surgery, • fascicular or bundle branch block, • –pericarditis, tamponade or fistulae
  42. 42. Take home message…. • IE is highly fatal condition with overall mortalities ranging from 20-40% mainly due to cardiac and neurological complication. • Patient present with Anemia Fever Splenomegaly and Clubbing : cardiac examination is mandatory. • Endocarditis is not just limited to valves. • High risk of suspicion with early diagnosis and treatment may affect the outcome favourably.

Editor's Notes

  • Also seen in trauma trichinosis,leukemia,scurvy psoriasis arthritis vasculitis
  • Aplastic anemia,leukemia,scurvy,HIV retinopathy