Infective Endocarditis**

Question 1

Infective Endocarditis

Answer 1

IE is characterised by colonisation or invasion of the heart valves or mural endocardium by a microbe, leading to the formation of bulky, friable vegetations composed of thrombotic debris and organisms, often associated with the destruction of the underlying cardiac tissues. Most cases are bacterial.

Question 2

How is IE classified?

Answer 2

• Acute
• Subacute

Question 3

Acute IE

Answer 3

Destructive infection, often in a previously normal heart valve, with a highly virulent organism. Difficult to cure with abx, usually require surgery, often leads to death.

*Staphylococcus aureus. *

Question 4

Subacute IE

Answer 4

Tends to be in a abnormal heart, particularly deformed valve by organism sof low virulence, that may appear insidiously and a protracted course over weeks to months.

*Staphylococcus viridians, *HACEK group - nromal flora of the oral cavity.

Question 5

Aetiology of IE

Answer 5

May occur on previously normal valves but more commonly on rheumatic fever damaged valves, myxomatous mitral valve, degenerative calcific valvular stenosis, bicuspid aortic valve or artificial (prosthetic) valves. The abnormal jets that cause platlet-fibrin deposits to accumulate, may be important in the pathognesis.

Question 6

Risk factors IE

Answer 6

• Neutropenia
• Immunodeficiency/immunosuppression
• Diabetes mellitus
• Alcohol
• IV drug use

Question 7

Macroscopic feature IE

Answer 7

Both acute and subacute lead to single or multiple friable, bulky and potantially destructive vegetations containing fibrin, inflammatory cells and bacteria or other organisms on the heart valves. Mitral and aortic are most common sites of infection - right side in IVDU.

Vegetations may erode into the underlying myocardium to produce an abscess (ring abscess).

Vegatations with subacute endocarditis are associated with less valvular destruction han those of acute endocarditis - these have granulation tissue at their bases. May ultimately become a chronic inflammatory infiltrate - fibrosis and calcification.

Question 8

Clinical feature of IE

Answer 8

Clinical features can be local and system.

Local

• Heart murmurs: 90% of patients with left-sided lesions (may relate to the preexisting cardiac abnormality or change in murmur).

Systemic

• Subacute infectious endocarditis: fever, non-specific fatigue, weight loss, flu-like symptoms.
• Acute infectious endocarditis: rapidly developing fever, chills, weakness, unwell.

Microemboli

• Petechiae
• Splinter haemorrhages
• Janeway lesions: erythematous or haemorrhagic non-tender lesions on the palms and soles
• Systemic emboli: brain, kidneys, myocardium, abscess may develop at the sites (septic infarcts).

Immunologically mediated

• Glomerulonephritis: caused by antigen-antibody complex deposition (rememebr to dipstick the urine for haematuria and send a ‘hot urine’ sample.
• Osler’s nodes: subcutaneous nodules in the pulp of the digits
• Roth spots: retinal haemorrhages

Question 9

Prevention of IE

Answer 9

*Prophylactic use of abx: *dental, surgical or other invasive procedure, int hose people with abnormal heart valves.

Question 10

Diagnosis of IE

Answer 10

Diagnosis is made based on the *New Modifies Duke Criteria. *

Pathologic critera

• Microorganisms demonstrated by culture or histological examination of a vegetation, a vegetation that has embolised, or an intracardiac abscess specimen; OR
• Pathologic lesions; vegetation or intracardiac abscess confirmed by histologic examination showing active endocarditis

Clinical criteria

• 2 major criteria; or
• 1 major criteria and 2 minor criteria; or
• 5 minor criteria

Major criteria

• Blood culture positive for IE:
  
  • Typical organisms consistent with IE from 2 separate blood cultures: *Viridians Streptococci, Streptococcus bovis, *nutritionally variant Streptococci, HACEK group, *Staphylococcus aureus; *or community-acquired enterococci, in the absence of a primary cous.
  • Microorganisms consistent with IE from persistently positive blood cultures defined as the following:
    
    • At least 2 positive cultures of blood samples drawn 12 hours apart; or
    • All of 3 or a majority of >4 separate cultures of blood (with first and last sample drawn at least one hour apart).
• Single positive culture for *Coxiella burnetti *or antiphase I IgE antibody titre of >1:800
• Evidence of endocardial involvement - echocardiogram positive for IE defined as follows:
  
  • Oscillating intracardiac mass on valve or supporting structures, in the path or regurgitant gets, or on implanted material in the absence of an alternative anatmomical explanation; or
  • Abscess; or
  • New partial dehiscence of prosthetic valve
• New valvular regurgitation (worsenign or changing of pre-existing murmur not sufficient).

Minor criteria

• Predisposition, predisposing heart condition or injection drug use
• Fever, temperature >38 degrees
• Vascula phenomena, major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhages, and Janeway lesions.
• Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots, and rheumatoid factor
• Microbial evidence: positive blood culture but does not meet a major criterion as noted above (excluding single positive cultures for coagulase-negative staphylococci and organisms that do not cause endocarditis) or serological evidence of active infection with organism consistent with IE.

Question 11

Non-bacterial thrombotic endocarditis

Answer 11

Also known as ‘marantic endocarditis’.

Small and sterile thrombi on the line of closure of the cardiac valve. Often in debilitated patients - hypercoagulable state seen in many cases - emboli are the major problem

Question 12

Libman-Sacks Disease

Answer 12

In teh CT disease systemic erythematosus, occasionally small sterile vegetations on the mitral and tricuspid valves.