015Endocarditis //
CONTENTS
140 Principles of Endocarditis
141 Native Valve Endocarditis
143 Complications of Native Valve Endocarditis
145 Right Heart Endocarditis
145 Prosthetic Valve Endocarditis
146 Pacemaker/Polymer-Associated Endocarditis
147 Non-Infective/Abacterial Endocarditis
148 Indications for Surgery
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NOTES PRINCIPLES OF ENDOCARDITIS
The prevalence of Definition endocarditis associated with prothetic valves and Endovascular microbial infection of cardiovascular structures pacemaker leads is on the increase. Location • Valves • Large intrathoracic vessels • Ventricular and atrial endocardium • Prosthetic material • Polymere associated structures (lines) • Eustachian valve
TRICUSPID VALVE ENDOCARDITIS – apical four- chamber view RV optimized/2D
Endocarditis with a large vegetation attached to the native tricuspid valve. Thickened leafl ets
TV vegetation
Vegetation is an infected Pathophysiology of Endocarditis mass attached to endocardial structures, such as valves or implanted intracardiac material. On 2D Embolism echo they frequently appear as oscillating structures of variable size Active infection and morphology.
Endocardial defect
Post endocarditis Non-significant Healing with Perforation endocardial lesion/ calcification/ fibrosis fibrosis/thickening
Principle of a ”super-infected” thrombus: The endothelial lesion initiates a repair process which involves thrombus formation. In the presence of bacteremia this thrombus may be super-infected. Further consequences include repair ad integrum, tissue destruction, embolism, and defect healing.
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PRINCIPLES OF ENDOCARDITIS NOTES
Microbiology Staph. aureus infection predisposes to abscess Other 14% formation and complications of Culture negative 17% Staph. aureus 25% endocarditis!
Staph. epidermidis 13% Enterococcus 11% Strept. bovis 20%
MITRAL VALVE ENDOCARDITIS AMVL – PLAX zoomed/2D
A vegetation is attached to the tip of the anterior mitral valve leaflet. Vegetation LA
Epidemiologic Facts on Endocarditis
• Large geographical variations in the • Increase in the elderly population incidence of endocarditis (3–10 • Sclerosis and aging also predispose to episodes/100.,000 person-years) endocarditis
NATIVE VALVE ENDOCARDITIS
Diagnosis, Symptoms and Findings Endocarditis may be manifested in many ways, many of which • Fever/night sweat may be atypical • Predisposing factors In the setting of infection, heart • Conjunctival petechiae murmur or atypical symptoms, • Janeway lesions Echo Culture think of endocarditis. Early • Roth spots diagnosis saves lives. • Splinter hemorrhages • Vegetations Blood culture and other signs of • Regurgitations Clinics infection (CRP, leukocytes, etc.) • Complications of endocarditis are equally important. A negative (abscessive destruction) blood culture does NOT rule out • Pericardial efusion endocarditis.
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NOTES NATIVE VALVE ENDOCARDITIS
MITRAL VALVE ENDOCARDITIS – TEE surgical view/3D Vegetation
Large vegetation on the posterior leaflet prolapsing into the left atrium
Posterior leaflet
Anterior leaflet
Follow-up studies help to make Differential Diagnosis an accurate diagnosis (progression?). • Fibrosis/calcification • Tangential imaging of structures • Myxomatous degeneration (e.g. mitral • Old vegetations valve prolapse) • Tumors/thrombi • Lambl‘s excrescence/strands
Transesophageal Indication for Transthoracic Echo in echocardiography is not Suspected Endocarditis mandatory in isolated right-sided native valve endocarditis with good Clinical Suspicion of Endocarditis transthoracic quality.
TTE
Prosthetic Poor quality Positive Negative TTE valve, intercardiac Persistent clinical suspicion device
High Low
TEE TEE Stop
If the initial TEE is negative but endocarditis is still suspected, repeat TEE within 7–10 days
ESC guidelines 2009
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NATIVE VALVE ENDOCARDITIS NOTES
What Else to Look For? ”Healing” usually leads to some degree of fibrosis or calcification • Involvment of other valves • Valve obstruction (large of the afected valve. • Regurgitations and resulting vegetations, rare) volume overload • Coronary embolization of • Myocardial function (right + left) vegetation leading to wall motion • Pericardial/pleural efusion abnormalites (rare)
COMPLICATIONS OF NATIVE VALVE ENDOCARDITIS
Complications Embolization is the primary manifestation of endocarditis in • Embolism • Pseudoaneurysm 28–47% of all patients. The risk • Valve destruction • Perforation of embolization depends on the • Regurgitation/heart failure • Fistula size (>10 mm) and mobility of • Abscess • Mycotic aneurysm the vegetation. Exclude endocarditis in the setting of stroke and fever.
Types of Valve Destruction
MV perforation Fistula
Valve perforation is a hole in the cusp or leaflet which appears as an interruption in endocardial tissue continuity, best seen with color Doppler. In contrast, a fistula is a communication with neighbouring cavities that does not directly involve the valve (for instance, between the aorta and the left atrium).
Pseudoaneurysm – MV pseudo- intervalvular aneurysm fibrosa
Pulsatile perivalvular (echo-free) cavity communicating with the cardiovascular lumen.
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NOTES COMPLICATIONS OF NATIVE VALVE ENDOCARDITIS
Types of Valve Destruction
AV ring abscess MV annular abscess
Perivalvular cavity filled with infectious material which has a non-homogeneous (echodense/echolucent) appearance
AV cusp MV flail leaflet rupture
Tear in the aortic cusp or chordal rupture, which usually leads to excentric regurgitation jets.
PSEUDOANEURYSM IN AV ENDOCARDITIS – TEE long-axis view/2D Pseudoaneurysm A pulsating cavity surounds the aortic valve (pseudoaneurysm). Numerous vegetations are pre- AV sent at the aortic cusps. Vegetation
Communication to the left ventricle
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RIGHT HEART ENDOCARDITIS NOTES
Causes of TV Endocarditis Tricuspid valve endocardits is very likely in patients with • Intravenous drug abuse • Indwelling catheters pulmonic abscess + drug abuse • Immunocompromised • Pacemaker + new heart murmur.
Tricuspid Valve Endocarditis – Facts Use atypical views to image • The most common organisms are • High recurrence rates. tricuspid valve endocarditis Staphylococcus aureus (60–80%) • Endocarditis frequently causes a flail and also look for pleural and Pseudomonas. tricuspid valve leaflet.. efusion (secondary to • Pulmonary hypertension, pulmonary • Tricuspid valve endocarditis may pulmonary infection). embolism or tricuspid regurgitation also occur in patients without may result in right heart failure. predisposing factors. • The prognosis is relatively good (10% inhospital mortality), but is poor in fungal infection.
Complications Tricuspid valve vegetations may become very large. • Valve destruction • Septic pulmonary embolism • Involvement of neighbouring cardiac • Lung abscess structures
PROSTHETIC VALVE ENDOCARDITIS
Risk Factors
• Heart failure • Valve degeneration • Wound complications • Prior history of endocarditis • Direct contamination during cardiac • Prosthesis thrombi (super-infection) surgery
Differential Diagnosis Prosthetic valve endocarditis is difcult to detect. • Artefacts • Strands Transesophageal echo is • Subvalvular residuals • Thrombus recommended in case of • Surgical materials • Hematoma suspicion. Find out which operation was Compare your findings with previous studies. performed, talk to the surgeon. Surgical material such as suture material or patches may mimic endocarditis.
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NOTES PROSTHETIC VALVE ENDOCARDITIS
Prosthetic valve endocarditis Complications is a life-threatening condition and is associated • Periannular abscess • Valve dehiscence with a poor prognosis. • Pseudoaneurysms • Valve obstruction • Paravalvular leaks • Fistula
PERIANNULAR PROSTHETIC VALVE ABSCESS – TEE short- axis/2D
The echodense area surounding AV the prosthesis corresponds to a vegetation periannular abscess. Additionally, a large vegetation is seen on the Abscess rim of the cusps.
PACEMAKER/POLYMER-ASSOCIATED ENDOCARDITIS
Pacemaker lead infection is Predisposing Factors difcult to diagnose. A negative study does not rule out • Pouch/Pocket infection • Diabetes endocarditis. Combine • Impaired immunity • The surgeon‘s experience transthoracic and • Systemic infection • Advanced age transesophageal echo to • Temporary pacing before implantation visualize as many portions of the leads as possible.
Clinical Presentation
• Fever, subfebrile (recurrent) • Septic shock (acute) • Pulmonary embolism • Poor general condition • Local complications
Lead infection usually Typical Sites of Infection occurs at sites where the leads are in contact • Vena cava superior • Tricuspid annulus with the endothelium. • Right atrium • Tricuspid valve
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PACEMAKER/POLYMER-ASSOCIATED ENDOCARDITIS NOTES
CENTRAL LINE ENDOCARDITIS Left atrium – apical four-chamber view/2D &TEE bicaval view/2D
Central line with its tip in the Vegetation right atrium. Mobile vegeta- Inf. Sup, vena cava tion attached to the catheter vena cava Mobile (thickened tip) on transthoracic structure echo (left) and the adjacent wall (right) seen in TEE. Catheter
Thickened catheter
NON-INFECTIVE/ABACTERIAL ENDOCARDITIS
Types • Libman-Sacks endocarditis • Marantic endocarditis • Antiphospholipid syndrome • Hypercoagulable state
Echo Characteristics
• Valve thickening • Small vegetations • Mild or moderate regurgitation • Pericardial efusion
Cardiac Manifestations of Libman-Sacks Endocarditis
• Valve thickening and vegetations • Left + right ventricular dysfunction • Mural thrombus • Pericardial efusion • Spontaneous contrast
LIBMAN-SACKS ENDOCARDITIS – Thickened apical three-chamber view/2D valve Patient with lupus and antiphos- pholipid syndrome. Several small vegetations are seen on the mitral valve.
Vegetations
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NOTES INDICATIONS FOR SURGERY
ESC Guidelines 2009
Recommendations for Surgery in Infective Endocarditis (IE)
Heart Failure Timing Class Level
Aortic or mitral IE with severe acute regurgitation or valve obstruction, causing refractory pulmonary Emergency I B edema or cardiogenic shock
Aortic or mitral IE with fistula into a cardiac chamber or pericardium causing refractory pulmonary edema or shock Emergency I B
Aortic or mitral IE with severe acute regurgitation or valve obstruction and persistent heart failure or echocardiographic signs of poor hemodynamic tolerance (early mitral closure or Urgent I B pulmonary hypertension)
Aortic or mitral IE with severe regurgitation and no HF Elective IIa B
Uncontrolled Infection
Locally uncontrolled infection (abscess, false aneurysm, fistula, enlarging vegetation) Urgent I B
Persistent fever and positive blood cultures > 7 – 10 days Urgent I B
Infection caused by fungi or multiresistant Urgent I B organisms elective
Prevention of Embolism
Aortic or mitral IE with large vegetations and one or more embolic Urgent I B episodes despite appropriate antibiotic therapy
Aortic or mitral IE with large vegetations (>10 mm) and other predictors of complicated Urgent I B course of disease (heart failure, persistent infection, abscess)
Isolated very large vegetations (>15 mm) Urgent IIb B
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