Heart on Fire: Infective Endocarditis. Objectives. Disclosure 8/27/2018. Mary McGreal DNP, RN, ANP-c, CCRN
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1 Heart on Fire: Infective Endocarditis Mary McGreal DNP, RN, ANP-c, CCRN Objectives Discuss the incidence of infective endocarditis? Discuss the pathogenesis of infective endocarditis? Discuss clinical manifestation of infective endocarditis? Discuss the diagnostic criteria for infective endocarditis and outline the treatment modalities? No disclosures Disclosure 1
2 Significance Infectious endocarditis (IE) is an uncommon and potentially lethal infection of the endocardial surface of the heart IE can present with very diverse clinical presentations which makes its diagnosis challenging It remains a therapeutic challenge with a high morbidity and mortality despite advances in medicine and surgery. The trend of IE has evolved to affect older patients with comorbidities and known structural heart disease Background IE affects up to 1500 people a year The male to female ratio is 2:1 May occur at any age, but it is increasingly common in the elderly Laing C, (2015). Understanding infective endocarditis Nursing Critical Care. 10:6-9 Infective Endocarditis 75 % of established cases occur in patients with structural defects Mitral valve most common (40%) Aortic valve (30)% Multi-valvular Tricuspid (5%) Rarely pulmonary valve Cahill T, et al. (2017). Challenges in infective endocarditis JACC. 69:3:
3 Classification Temporal evolution of the disease Acute Rapid onset Fever Subacute Insidious onset Low grade fever, Malaise Weight loss Location of the infection Native valve endocarditis (NVE) Preexisting heart lesion--- MVP and AS Prosthetic valve endocarditis (PVE) Early PVE within 60 days of surgery Device related endocarditis Right sided endocarditis IVDA Pathophysiology IE is the result of a complex interaction that occurs between the causative organism and the host The cardiac endocardium is resistant to infection, as long as it remains intact It is damaged due to turbulent blood flow caused by a dysfunctional valve or due to the introduction of invasive devices such as catheters, sheaths or pacing wires Bruno Hoen (2013). Infective Endocarditis NEJM: 368; 15:
4 Venturi Effect A Venturi effect is produced, when fluid is driven from a high-pressure source through a narrow orifice into a lowpressure sink. The atrial side of mitral and tricuspid valves and ventricular sides of aortic and pulmonary valves are most frequently involved in IE Turbulence and the jet effect cause trauma to the endothelium in the lowpressure sink immediately beyond the orifice Hence the perfect breeding ground for IE to develop Venturi Effect Cahill T, et al. (2017). Challenges in infective endocarditis JACC. 69:3: Causative Organisms Cahill T, et al. (2017). Challenges in infective endocarditis JACC. 69:3: Bacterial Causes of Different Types of Endocarditis CAUSATIVE ORGANISM NATIVE VALVE ENDOCARDITIS INTRA-VENOUS DRUGABUSE Right Sided Left Sided Less than 12 months PROSTHETIC VALVE ENDOCARDITIS More than 12 months S. AUREUS 42% 77% 23% 25% 17% STREPTOCOCCI 29% 5% 15% 2% 28% ENTEROCOCCI 11% 2% 24% 10% 14% GRAM-NEGATIVE BACILLI 2% 5% 13% 13% 5% FUNGI 2% 12% 8% 2% HACEK GROUP 2% 4% POLYMICROBIALS 1% 8% 10% 3% 5% CULTURE NEGATIVE 8% 3% 3% 8% 9% Laing C, (2015). Understanding infective endocarditis. Nursing Critical Care. 10:6-9 4
5 Laing C, (2015). Understanding infective endocarditis. Nursing Critical Care. 10:6-9 Clinical Manifestations Most of the signs and symptoms of IE are due to four mechanisms: Infection of the endocardial layer of the heart and associated damage to the valves Release of infected vegetation (septic emboli) that forms an emboli and blocks blood flow to organs and tissue Continuous shedding of bacteria continuous bacteremia The formation of immune complexes between the cells of the immune system +causative organisms Clinical Manifestations Cont d Heart Murmur Septic emboli Left sided valves involved Vegetations > 10 mm Mitral valve is affected Staph. Aureus Brain, spleen, kidney, bowel most common organs affected Frequency decreases once effective antibiotics are started 5
6 Clinical Manifestations Cont d Neurological Mycotic aneurysms Peripheral (constant shedding of bacteria in to bloodstream) Petechiae Splinter hemorrhage Roth s spots Osler s nodes Janeway lesions. Clinical Manifestations Cahill T, et al. (2017). Challenges in infective endocarditis JACC. 69:3: Diagnosis IE is a disease that presents with some subtleness, and can be difficult to diagnosis Osler s description of endocarditis in Few diseases present greater difficulties in the way of diagnosis than malignant endocarditis (such that) fully one half the diagnosis was made post-mortem 6
7 Diagnosis Cont d It requires a combination of clinical, microbiological and echocardiography results Clinical H&P Microbiological 3 sets of blood cultures Sampling should be obtained from a peripheral vein Incubation period of blood cultures 5 days Echocardiography Echo confirms and measures vegatations, detects intracardiac compliance, and assess cardiac function TTE/TEE The echo data that is given diagnostic weight within the Duke criteria is very specific: Mobile echo dense masses attached to valvular leaflets or endocardial walls Periannular abscesses New dehiscence of a valvular prosthesis Modified Dukes Criteria Established in 1994 by the Duke Endocarditis Society and revised in 2000 It is divided into major and minor criteria Three possible results based on the number of major and minor criteria that are present or not: Definite IE 2 major criteria or 1 major and 3 minor criteria or 5 minor criteria Possible IE 1 major +1 minor or 3 minor Rejected IE Alternate diagnosis established Symptoms resolved with 4 days of antimicrobial therapy If surgery/autopsy reveal no histological evidence of IE 7
8 Modified Dukes Infective Endocarditis Criteria Clinical Criteria 2 Major criteria or 1 major and 3 minor criteria or 5 minor criteria Definition of terms Major Criteria Positive blood cultures Evidence of endocardial involvement (TTE&TEE) Minor Criteria Predisposition (previous endocarditis, predisposing heart condition, IVD) Fever (temperature >38 C) Vascular phenomena (emboli) Immunologic phenomena (Osler nodes) Microbiological evidence (positive BC not met in major criteria characteristics) Treatment The major goals therapy for IE are: Eradicate the infection Address the complications Antibiotics Treatment for heart failure Hemodialysis Surgical intervention Anticoagulation Therapy Although thrombosis is a key element of IE Anticoagulation is controversial Evidence indicates worse outcomes for patients who are anticoagulated than those who are not If an established reason for anticoagulation exists A standard regimen of anticoagulation should be followed 8
9 Surgical Treatment 15-20% od patients with IE are treated surgically Indications Heart Failure --- valvular dysfunction Antibiotic therapy failure Persistent vegetation after systematic embolization Increase in vegetation size after antimicrobial therapy Neurological complications Prevention of Infective Endocarditis Oral hygiene Gingivitis is a common source of spontaneous bacteremias Consider prophylaxis against IE in patients with: Presence of prosthetic heart valve History of endocarditis Cardiac transplant patient who develop cardiac valvulopathy Congenital heart disease with a high-pressure gradient lesion Coronary artery stent is not considered to place the patient at high risk for endocarditis Implication for Practice IE is a devastating illness Identifying the causative microorganism is central to diagnosis and appropriate treatment Indications for antibiotic prophylaxis have been restricted to patients with a prosthetic valve or a history of IE 9
10 References Baddour L, Wilson W, Bayer A, et al. (2015). Infective endocarditis in adults: diagnosis, antimicrobial therapy, and management of complications: a scientific statement for healthcare professionals from the American Heart Association. Circulation.132: Bruno Hoen (2013). Infective Endocarditis. NEJM: 368;15: Cahill T, Baddour L, Habib G, et al. (2017). Challenges in infective endocarditis. JACC. 69:3: Erwin J, Otto C. (2014). Infective endocarditis: old problem, new guidelines and still much to learn. Heart. 100: Kang D. (2015). Timing of surgery in infective endocarditis Heart.101: Laing C, (2015). Understanding infective endocarditis. Nursing Critical Care. 10:6-9 10
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