1. Jim Czarnecki, D.O. Internal Medicine Lecture Series
Endocarditis
Jim Czarnecki, D.O.
Internal Medicine Lecture Series

2. Introduction

3. Background
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.
Three types:
Native valve (acute and subacute)
Prosthetic valve (early and late)
Related to intravenous drug use

4. Native Valve Endocarditis

5. Native Valve Endocarditis
Usually has an aggressive course
Typical causative agents are Staphlococcus aureus and group B streptococci.
Underlying structural valve disease may not be present.
Subacute endocarditis usually has a more indolent course than the acute form.

6. Native Valve Endocarditis
Alpha-hemolytic streptococci or enterococci, usually in the setting of underlying structural valve disease, typically are the causative agents of this type of endocarditis.

7. Prosthetic Valve Endocarditis

8. Prosthetic Valve Endocarditis
Early prosthetic valve endocarditis occurs within 60 days of valve implantation.
Staphylococci, gram-negative bacilli, and Candida species are the common infecting organisms.

9. Prosthetic Valve Endocarditis
Late prosthetic valve endocarditis occurs 60 days or more after valve implantation.
Alpha-hemolytic streptococci, enterococci, and staphylococci are the common causative organisms.

10. Endocarditis and IV Drug Use

11. Endocarditis and IV Drug Use
Commonly involves the tricuspid valve.
S. aureus is the most common causative organism.

12. Pathophysiology

13. Pathophysiology
Infective endocarditis generally occurs as a consequence of nonbacterial thrombotic endocarditis, which results from turbulence or trauma to the endothelial surface of the heart
Transient bacteremia then leads to seeding of lesions with adherent bacteria, and infective endocarditis develops.

14. Pathophysiology
Pathologic effects due to infection can include local tissue destruction and embolic phenomena.
Secondary autoimmune effects, such as immune complex glomerulonephritis and vasculitis, can occur.

15. Frequency

16. Frequency
In the US: Incidence is 1.4 to 4.2 cases per 100,000 people per year.
Internationally: Incidence of disease appears to be similar throughout the developed world.

17. Mortality / Morbidity

18. Mortality / Morbidity Increased mortality rates are associated with:
Increased age
Infection involving the aortic valve
Development of congestive heart failure
Central nervous system (CNS) complications
Underlying disease
Mortality rates also vary with the infecting organism.

19. Mortality / Morbidity
Mortality rates in native valve disease range from 16-27%
Mortality rates in patients with prosthetic valve infections are higher.
More than 50% of these infections occur within 2 months after surgery.

20. Gender / Age

21. Gender / Age Gender: Age:
The male-to-female ratio is approximately 2:1
Age:
Can occur at any age
Mean age of patients has gradually risen over the past 50 years
Currently, more than 50% of patients are older than 50 years of age.

22. Clinical Aspects

23. History

24. History Present illness history is highly variable.
Symptoms are commonly:
Vague
Emphasize constitutional complaints
May focus on primary cardiac effects
Secondary embolic phenomena

25. History
May present with signs of congestive heart failure (due to valvular insufficiency)
Secondary phenomena could include focal neurological complaints due to:
Embolic stroke
Back pain associated with vertebral osteomyelitis
Fever and chills are the most common symptoms.

26. History (Other) Other common complaints include:
Anorexia
Weight loss
Malaise
Headache
Myalgias
Additional common complaints include:
Night sweats
Shortness of breath
Cough
Joint pains

27. Physical

28. Physical
Fever, either low-grade or intermittent, is present in 90% of patients.
Heart murmurs are heard in approximately 85% of patients.
Signs of neurologic disease occur in as many as 40% of patients.
Embolic stroke with focal neurologic deficits is the most common etiology. Others can be intracerebral hemorrhage and multiple microabscesses.

29. Physical
Signs of systemic septic emboli are due to left heart disease and are more commonly associated with mitral valve vegetations.
Multiple congestive heart failure signs, such as distended neck veins, are frequently due to acute left-sided valvular insufficiency.

30. Physical
Classic signs of infective endocarditis are found in as many as 50% of patients. They include:
Petechiae – common by nonspecific finding
Splinter hemorrhages – dark red linear lesions in the nailbeds
Osler nodes – Tender subcuaneous nodules usually found on the distal pads of the digits
Janeway lesions – Nontender maculae on the palms and soles
Roth spots – Retinal hemorrhages with small, clear centers; rare and observed in only 5% of patients.

31. Petechiae

32. Splinter Hemorrhages

33. Osler Nodes

34. Osler Nodes

35. Janeway lesions

36. Roth Spots

37. Physical (Other) Other findings: Additional findings: Splenomegaly
Stiff neck
Delirium
Paralysis
Hemiparesis
Aphasia
Conjunctival hemorrhage
Additional findings:
Pallor
Gallops
Rales
Cardiac arrhythmia
Pericardial rub
Pleural friction rub

38. Causes

39. Causes: Native Valve

40. Causes: Native Valve
Rheumatic valvular disease (30%) – primarily involves the mitral valve followed by the aortic valve.
Congenital heart disease (15%) – include patent ductus arteriosus, ventricular septal defect, tetralogy of Fallot
Mitral valve prolapse with associated murmur (20%)

41. Causes: Native Valve
Degenerative heart disease – includes calcific aortic stenosis due to bicuspid valve, Marfan syndrome, or syphilitic disease
Approximately 70% of cases are caused by Streptococcus species including Streptococcus viridans, Streptococcus bovis, and enterococci.
Staphlococcus species cause 25% of cases and generally demonstrate a more aggressitve acute course.

42. Causes: Prosthetic Valve

43. Causes: Prosthetic Valve
Early disease, presenting shortly after surgery, has a different bacteriology and prognosis than late disease, which presents in a subacute fashion similar to native valve endocarditis.
Infection associated with aortic valve prostheses is particularly associated with local abscess and fistula formation.
This may lead to heart block, shunting of blood to the right atrium, or pericardial tamponade.

44. Causes: Prosthetic Valve
Endocarditis can occur in association with intravascular devices.
Infection that occurs early after surgery may be caused by a variety of pathogens, including S. aureus and S. epidermidis.
Late disease is most commonly caused by streptococci.

45. Causes: IV Drug Use

46. Causes: IV Drug Use
Most commonly involves the tricuspid valve, followed by the aortic valve.
Two thirds of patients have no previous history of heart disease and no murmur on admission.
Diagnosis of endocarditis in intravenous drug users can be difficult and requires a high index of suspicion.

47. Causes: IV Drug Use
S. aureus is the most common (<50% of cases) etiologic organism. Other causative organisms include streptococci, fungi, and gram-negative rods (eg. Pseudomonads, Serratia species).

48. Causes: Fungal Endocarditis
Found in intravenous drug users and intensive care unit patients who receive broad-spectrum antibiotics.
Blood cultures are often negative, and diagnosis frequently is made after microscopic examination of large emboli.

49. Causes: Diagnosis
Usually made using Duke Criteria (link is on IM website). Major criteria include:
Multiple positive blood cultures for the infecting organism
Echocardiographic evidence of endocardial involvement or a new regurgitant murmur on physical examination

50. Differentials

51. Differentials Connective tissue disease Fever of unknown origin
Intra-abdominal infections
Septic pulmonary infection
Tricuspid regurgitation

52. Workup

53. Lab Studies Send baseline studies: CBC Electrolytes Creatinine BUN
Glucose
Coagulation Panel

54. Lab Studies
Two sets of blood cultures have greater than 90% sensitivity when bacteremia is present.
Anemia of chronic disease is common in subacute endocarditis
ESR, while not specific, is elevated in more than 90% of cases.
Proteinuria and microscopic hematuria are present in approximately 50% of cases.

55. Lab Studies Leukocytosis is observed in acute endocarditis
Anemia is present in subacute endocarditis.
Rheumatoid factor is noted in subacute endocarditis.
Serology for Chlamydia, Q fever (Coxiella), and Bartonella may be useful in culture-negative endocarditis.

56. Imaging Studies Echocardiography
Transthoracic echocardiography has a sensitivity of approximately 60%.
Transesophageal echocardiography has a sensitivity of more than 90% for valvular lesions.
Both techniques are highly specific for valvular vegetations.

57. Vegetation on Mitral Valve

58. Imaging Studies
Imaging studies are particularly indicated with culture-negative cases, such as in fungal endocarditis.
Echocardiography is highly useful to assess local complications, such as abscesses.
Chest radiography: Pulmonary embolic phenomena strongly suggest tricuspid disease.
Ventilation/perfusion (V/Q) scanning: This may be useful in right-sided endocarditis.
CT scanning: helpful in localizing abscesses.

59. Imaging Studies
EKG:
Nonspecific changes are common
First-degree AV block and new interventricular conduction delays may signal septal involvement in aortic valve disease; both are poor prognostic signs.
Cardiac catheterization – indicated to determine the degree of valvular damage.

60. Treatment

61. Treatment
Focus is on making the correct diagnosis and stabilizing the patient with acute disease and cardiovascular instability
Most cases the etiologic microbial agent is not known
General recommendations: three (3) sets of blood cultures over a few hours, and then empiric antibiotic therapy may be administered.

62. Treatment General Measures: Consultations:
Treatment of congestive heart failure
Oxygen
Hemodialysis (may be required in patients with renal failure)
Consultations:
Cardiology
Cardiothoracic Surgery Service
Infectious Diseases Service

63. Medication

64. Medication
Empiric antibiotic therapy is chosen based on the most likely infecting organism.
Native valve disease usually is treated with penicillin G and gentamicin for synergistic treatment of streptococci.
Patients with history of IV drug use – treated with nafcillin and gentamicin to cover methicillin-sensitive straphylococci.

65. Medication
Infection of a prosthetic valve may include methicillin-resistant Staphylococcus aureus – thus vancomycin and gentamicin may be used.
Rifampin also may be helpful in patients with prosthetic valves or other foreign bodies; however, it should be used in addition to vancomycin or gentamicin.

66. Follow-up

67. Deterrence / Prevention
Consider prophylaxis against infective endocarditis in patients at high risk:
Presence of prosthetic heart valve
History of endocarditis
History of rheumatic heart disease
Congenital heart disease with a high-pressure gradient lesion and mitral valve prolapse with a heart murmur

68. Deterrence / Prevention
The presence of coronary artery stenting is not considered to place the patient at high risk for endocarditis.

69. Deterrence / Prevention
Consider prophylaxis in patients before they undergo procedures that may cause transient bacteremia, such as:
Ear, nose, and throat (ENT) procedures associated with bleeding, including dental manipulations and nasal packing
Incision and drainage of an abscess
Anoscopy and Foley catheter placement when a urinary tract infection is present or suspected

70. Complications

71. Complications Myocardial infarction, pericarditis, cardiac arrhythmia
Cardiac valvular insuffiency
Congestive heart failure
Sinus of Valsalva aneurysm
Aortic root or myocardial abscesses
Arterial emboli, infarcts, mycotic aneurysms
Arthritis, myositis
Glomerulonephritis; acute renal failure
Stroke syndromes
Mesenteric or splenic abscess or infarct

72. Prognosis

73. Prognosis
Acute endocarditis due to S. aureus is associated with a high mortality rate (40%), except when it is associated with IV drug use.
Endocarditis due to streptococci has a mortality rate of approximately 10%.
Prognosis largely depends on whether or not complications develop.

74. Competency Exam

75. Question One 1) Signs of systemic septic emboli are associated with:
Pulmonic valve vegetations
Mitral valve vegetations
Tricuspid valve vegetations
Aortic valve vegetations
All valves of the heart

76. Question One 1) Signs of systemic septic emboli are associated with:
Pulmonic valve vegetations
Mitral valve vegetations
Tricuspid valve vegetations
Aortic valve vegetations
All valves of the heart

77. Question Two
2) All are true of IV drug use-induced endocarditis, except:
Involves tricuspid valve
Involves the aortic valve
Can be difficult to diagnosis
Streptococci species is usually the etiologic organism
There is usually no murmur on admission.

78. Question Two
2) All are true of IV drug use-induced endocarditis, except:
Involves tricuspid valve
Involves the aortic valve
Can be difficult to diagnosis
Streptococci species is usually the etiologic organism
There is usually no murmur on admission.

79. Question Three 3) Pulmonay embolic phenomena strongly suggest:
Pulmonic valve disease
Mitral valve disease
Tricuspid valve disease
Aortic valve disease
Does not involve any heart valves

80. Question Three 3) Pulmonay embolic phenomena strongly suggest:
Pulmonic valve disease
Mitral valve disease
Tricuspid valve disease
Aortic valve disease
Does not involve any heart valves

81. Thank you for your attendance.
End of Lecture
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