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INFECTIVE ENDOCARDITIS
Prepared by
B.ABHISHEK
PHARM . D
Definition
Infective Endocarditis (IE) is an inflammation of
the endocardium, the membrane lining the chamber of
the heart and covering the cups of heart valves.
Most commonly it refers to infection of heart
valves by various microbes
Epidemiology
In the world, 3-7.5 % people per 1, 00,000 in a year
are affecting with Infective Endocarditis
In India, native valve endocarditis due to
streptococcus species and observed in 30-
65% of population
Acute
Fulminating form
High fever and systemic toxicity is observed
Mostly occurs due to Staphylococcus aureus
If not untreated, it leads to death
Sub acute infection
Indolent form
Mostly occurs due to Viridians streptococci
Usually occurs in persons with pre existing valvular disease
Prosthetic Valve Endocarditis (PVE)
Infection to the endocardium occurs following insertion of prosthetic heart valve
Native Valve Endocarditis (NVE): Infection to a previously normal heart valve
Cardiac Device Infective Endocarditis (CDIE)
Infection to endocardium occurs following insertion of cardiac implantable electronic
device
Classification
Risk factors
Presence of prosthetic valve
Previous Endocarditis
Health care related exposure
Congenital heart disease
Chronic IV access
Diabetes mellitus
Acquired valvular dysfunction
Cardiac implantation device
Chronic heart failure
Mitral valve prolapse with regurgitation
Intravenous drug abuse
Etiology
Streptococci species
Staphylococci species
Enterococci species
Gram negative aerobic bacilli
Fungi
HACEK organisms – Haemophilus,Aggregatibactor,
Cardiobacterium, Eikenella, Kingella.
Pathophysiology
Stigmata of Endocarditis
General
Fever
Chills
Weakness
Dyspnoea
Night sweats
Weight loss
Malaise
Osler’s nodes
Janeway’s lesions
Splinter haemorrhages
Petechiea
Clubbing of fingers
Roth’s spots
Flank pain with hematuria (Renal
artery Emboli)
Abdominal pain (Splenic artery
emboli)
Hemiplegia with altered mental
status (cerebral artery emboli)
Clinical presentation
Complications
Acute heart failure
Pulmonary abscess
Abscess in brain, kidney and spleen
Glomerularnephritis
Aneurysms
Cerebral infarction
Skin manifestations
Diagnosis
Clinical presentation
Lab tests
Echocardiography
Duke’s diagnostic criteria
Duke’s Criteria
Major criteria:
1. Blood culture positive
At least two positive cultures of blood samples drawn greater than
12hours apart
Single positive blood culture for coxiella burnetii
Antiphase 1 immunoglobulin G antibody titre greater than 1: 800
2. Evidence of endocardial involvement
Transesophageal echocardiography or transthorasic
echocardiography shows evidence of oscillating intracardiac mass on
valve or supporting structures or abscess or new partial dehiscence of
prosthetic valve
Minor criteria:
1. Predisposing heart problem
2. Injection drug use
3. Fever greater than 100.4 ͦ
F
4. Vascular phenomenon
Major arterial emboli
Septic pulmonary infarcts
Mycotic aneurysms
Intracranial hemorrhage
Conjuctival hemorrhage
Janeway’s lesions
5. Immunological phenomenon
Glomerularnephritis
Osler’s nodes
Roth’s spots
Rheumatoid factor
6. Microbial evidence of positive blood culture but does not meet above major criteria (HACEK)
Haemophilus species
Aggregate species
Cardiobacterium
Eikenella species
Kingella species
Duke’s criteria Interpretation
Definitive
 2 major criteria or
 5 major criteria or
 1 major criteria + 3 minor criteria
Possible
 1 major criteria + 3 minor criteria or
 3 minor criteria
Rejected
 If not met above criteria or
 Resolution of Infective Endocarditis with antibiotic therapy within 4 days or
 No pathological evidence
Non Pharmacological Treatment
Valvectomy and valvular replacement to remove infected
tissue
Treatment Algorithm of Infective Endocarditis
Drugs used in Treatment of Infective Endocarditis
Drug Category Mode of Action Dose Adverse Effects
Pencillin G Pencillins Inhibit bacterial cell
wall synthesis
3 million units-
IV-for every 4-6
hours
 Pseudomembranous colitis
 Maculopapular eruption
 Urticaria
 Serum sickness reaction
 Jarisch-Herxheimer reaction
Ampicillin Pencillins Inhibit bacterial cell
wall synthesis
2g-IV-for every
4 hours
 Erythema multiforme
 Urticaria
 Black hairy tongue
 Pseudomembranous colitis
 Seizures
Oxacillin Pencillins Inhibit bacterial cell
wall synthesis
2g-IV-for every
4 hours
 Diarrhea
 Rashes
 Fever
 Eosinophilia
 Hepatotoxicity
Ceftrioxone Cephalosporin Inhibit
bacterial cell
wall synthesis
2g-IV-for
every 12
hours
 Injection site reactions
 Eosinophilia
 Diarrhhea
 Thrombocytosis
 Transaminitis
Cefepime Cephalosporin Inhibit
bacterial cell
wall synthesis
2g-IV-for
every 8
hours
 Rashes
 Erythema
 Diarrhhea
 Transaminitis
 Hypophosphotemia
Gentamicin Aminoglycoside Inhibit
bacterial
protein
synthesis
3mg/kg-IV-
for 24 hours
 Vertigo
 Ataxia
 Increased creatinine levels
 Edema
 Erythema
Vancomycin Glycopeptides Inhibit bacterial
cell wall
synthesis
15-20mg/kg for
every 12-24
hours
 Hypersensitivity
 SJS reaction
 Increased creatinine levels
 Vertigo
 Pseudomembranous colitis
Daptomycin Lipopeptides Inhibit bacterial
protein, DNA,
RNA synthesis
≥8mg/kg-IV for
every 24 hours
 Insomnia
 Throat pain
 Chest pain
 Abdominal pain
 Edema
Rifampin Antitubercular
drug
Inhibit DNA
dependent RNA
polymerase
which inhibit
RNA
transcription
300 mg IV or po
every 8 hours
 Transaminitis
 Rashes
 Epigastric distress
 Anorexia
 Pseudomembranous colitis
Linezolid Mislleaneous
antibiotic
Inhibit protein
synthesis in
bacteria
600 mg IV or po
every 12 hours
 Diarrhea
 Taste alteration
 Discoloration of tongue
 Fungal infections
 Transaminitis
Resources
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC49434
30/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC49719
93/pdf/ACA-19-551.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC51060
88/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC50673
87/pdf/main.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC61167
10/pdf/main.pdf

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Endocarditis.pptx

  • 2. Definition Infective Endocarditis (IE) is an inflammation of the endocardium, the membrane lining the chamber of the heart and covering the cups of heart valves. Most commonly it refers to infection of heart valves by various microbes
  • 3.
  • 4. Epidemiology In the world, 3-7.5 % people per 1, 00,000 in a year are affecting with Infective Endocarditis In India, native valve endocarditis due to streptococcus species and observed in 30- 65% of population
  • 5. Acute Fulminating form High fever and systemic toxicity is observed Mostly occurs due to Staphylococcus aureus If not untreated, it leads to death Sub acute infection Indolent form Mostly occurs due to Viridians streptococci Usually occurs in persons with pre existing valvular disease Prosthetic Valve Endocarditis (PVE) Infection to the endocardium occurs following insertion of prosthetic heart valve Native Valve Endocarditis (NVE): Infection to a previously normal heart valve Cardiac Device Infective Endocarditis (CDIE) Infection to endocardium occurs following insertion of cardiac implantable electronic device Classification
  • 6. Risk factors Presence of prosthetic valve Previous Endocarditis Health care related exposure Congenital heart disease Chronic IV access Diabetes mellitus Acquired valvular dysfunction Cardiac implantation device Chronic heart failure Mitral valve prolapse with regurgitation Intravenous drug abuse
  • 7. Etiology Streptococci species Staphylococci species Enterococci species Gram negative aerobic bacilli Fungi HACEK organisms – Haemophilus,Aggregatibactor, Cardiobacterium, Eikenella, Kingella.
  • 9.
  • 10.
  • 11. Stigmata of Endocarditis General Fever Chills Weakness Dyspnoea Night sweats Weight loss Malaise Osler’s nodes Janeway’s lesions Splinter haemorrhages Petechiea Clubbing of fingers Roth’s spots Flank pain with hematuria (Renal artery Emboli) Abdominal pain (Splenic artery emboli) Hemiplegia with altered mental status (cerebral artery emboli) Clinical presentation
  • 12.
  • 13. Complications Acute heart failure Pulmonary abscess Abscess in brain, kidney and spleen Glomerularnephritis Aneurysms Cerebral infarction Skin manifestations
  • 15. Duke’s Criteria Major criteria: 1. Blood culture positive At least two positive cultures of blood samples drawn greater than 12hours apart Single positive blood culture for coxiella burnetii Antiphase 1 immunoglobulin G antibody titre greater than 1: 800 2. Evidence of endocardial involvement Transesophageal echocardiography or transthorasic echocardiography shows evidence of oscillating intracardiac mass on valve or supporting structures or abscess or new partial dehiscence of prosthetic valve
  • 16. Minor criteria: 1. Predisposing heart problem 2. Injection drug use 3. Fever greater than 100.4 ͦ F 4. Vascular phenomenon Major arterial emboli Septic pulmonary infarcts Mycotic aneurysms Intracranial hemorrhage Conjuctival hemorrhage Janeway’s lesions 5. Immunological phenomenon Glomerularnephritis Osler’s nodes Roth’s spots Rheumatoid factor 6. Microbial evidence of positive blood culture but does not meet above major criteria (HACEK) Haemophilus species Aggregate species Cardiobacterium Eikenella species Kingella species
  • 17. Duke’s criteria Interpretation Definitive  2 major criteria or  5 major criteria or  1 major criteria + 3 minor criteria Possible  1 major criteria + 3 minor criteria or  3 minor criteria Rejected  If not met above criteria or  Resolution of Infective Endocarditis with antibiotic therapy within 4 days or  No pathological evidence
  • 18. Non Pharmacological Treatment Valvectomy and valvular replacement to remove infected tissue
  • 19.
  • 20. Treatment Algorithm of Infective Endocarditis
  • 21.
  • 22.
  • 23.
  • 24.
  • 25.
  • 26.
  • 27. Drugs used in Treatment of Infective Endocarditis Drug Category Mode of Action Dose Adverse Effects Pencillin G Pencillins Inhibit bacterial cell wall synthesis 3 million units- IV-for every 4-6 hours  Pseudomembranous colitis  Maculopapular eruption  Urticaria  Serum sickness reaction  Jarisch-Herxheimer reaction Ampicillin Pencillins Inhibit bacterial cell wall synthesis 2g-IV-for every 4 hours  Erythema multiforme  Urticaria  Black hairy tongue  Pseudomembranous colitis  Seizures Oxacillin Pencillins Inhibit bacterial cell wall synthesis 2g-IV-for every 4 hours  Diarrhea  Rashes  Fever  Eosinophilia  Hepatotoxicity
  • 28. Ceftrioxone Cephalosporin Inhibit bacterial cell wall synthesis 2g-IV-for every 12 hours  Injection site reactions  Eosinophilia  Diarrhhea  Thrombocytosis  Transaminitis Cefepime Cephalosporin Inhibit bacterial cell wall synthesis 2g-IV-for every 8 hours  Rashes  Erythema  Diarrhhea  Transaminitis  Hypophosphotemia Gentamicin Aminoglycoside Inhibit bacterial protein synthesis 3mg/kg-IV- for 24 hours  Vertigo  Ataxia  Increased creatinine levels  Edema  Erythema
  • 29. Vancomycin Glycopeptides Inhibit bacterial cell wall synthesis 15-20mg/kg for every 12-24 hours  Hypersensitivity  SJS reaction  Increased creatinine levels  Vertigo  Pseudomembranous colitis Daptomycin Lipopeptides Inhibit bacterial protein, DNA, RNA synthesis ≥8mg/kg-IV for every 24 hours  Insomnia  Throat pain  Chest pain  Abdominal pain  Edema Rifampin Antitubercular drug Inhibit DNA dependent RNA polymerase which inhibit RNA transcription 300 mg IV or po every 8 hours  Transaminitis  Rashes  Epigastric distress  Anorexia  Pseudomembranous colitis Linezolid Mislleaneous antibiotic Inhibit protein synthesis in bacteria 600 mg IV or po every 12 hours  Diarrhea  Taste alteration  Discoloration of tongue  Fungal infections  Transaminitis