Download Free Medical Infectious heart diseases PowerPoint Presentation

Infectious heart diseases PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Endocarditis, which is titled "Infectious heart diseases", to know about the infectious diseases of the heart including infective endocarditis, myocarditis, and pericarditis.

Tags : Endocarditis, Infectious heart diseases, infective endocarditis, myocarditis, pericarditis

Published on : Jul 01, 2021 | Views : 2950 | Downloads : 3

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Infectious heart diseases Jiri Bonaventura, MD Department of Cardiology, Charles University in Prague, 2nd Faculty of Medicine and Motol University Hospital, Prague, Czech Republic
Slide 2-

Infectious diseases of the heart • Infective endocarditis • Myocarditis • Pericarditis
Slide 3-

Infective endocarditis
Slide 4-

Epidemiology IE is a relatively rare but serious disease with high mortality despite the improvement in dg. and th. Estimated annual incidence 3-10/100 000 The profile of patients and pathogens has changed over time (rheumatic fever x PM/ICD) Predisposing factors: prosthetic valves elderly patients with degenerated valves i.v. drug users i.v. catheters, pacemaker electrodes
Slide 5-

Classification • (Acute x subacute/ lenta) • NVE - native valve endocarditis • PVE - prosthetic valve endocarditis • IVDU - intravenous drug users • IE on PM / ICD electrodes
Slide 6-

Classification • Relapse - repeat IE within 6 months and proven identical pathogen • Reinfection, - new microorganism, or the same species but > 6 months • Early PVE - within 1 year (usually aggressive nosocomial infection of sewing material) • Late PVE - > 1 year after surgery/implantation
Slide 7-

Pathophysiology • IE is rare in healthy individuals despite common bacteremia (dental procedures, toothbrushing…) x • Any injury to endocardial surface (degenerative changes, impact of catheters, electrodes, prosthetic materials…) → endocardial damage, exposing EC matrix → factor III, platelet activation, fibrin-platelet (sterile) vegetation → increase risk of bacterial seeding
Slide 8-

NVE Rheumatic valvular disease – usually mitral valve followed by the aortic valve Congenital heart disease - patent ductus arteriosus, ventricular septal defect, tetralogy of Fallot (TOF), any native or surgical high-flow lesion Mitral valve prolapse Degenerative heart disease aortic stenosis in elderly ,bicuspid valve, Marfan syndrome, rarely syphilitic disease mitral regurgitation
Slide 9-

Clinical presentation • Variable! • Fever (95%), signs of systemic disease (nausea, weight loss….) • Heart murmur (85%) • Septic embolization (20-50%) brain, kidneys, spleen pulmonary • Peripheral microembolization less common
Slide 10-

Diagnostic testing 3 sets (aero + anaerobe) at different times + from diff. sites 85-90% - streptococci, staphylococci, enterococci 10% culture negative (usually due to previous ATB th.) less commonly HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella ) Fungi – Candida, Aspergillus Intracellular pathogens: Coxiella, Bartonella, Chlamydia, Mycoplasma, Legionella, Trephonema Blood cultures
Slide 11-

Diagnostic testing Echocardiography • TTE - low sensitivity (40-60%) • TEE - sensitivity 90 - 100% • vegetations / abscess / new prosthetic valve dehiscence = specific • new regurgitation / obstruction = not specific
Slide 12-

ppt slide no 12 content not found
Slide 13-

Duke criteria (IE probability) ESC guidelines 2015
Slide 14-

Duke criteria (IE probability)
Slide 15-

ppt slide no 15 content not found
Slide 16-

ppt slide no 16 content not found
Slide 17-

Treatment • ATB therapy • Surgery - performed in high-risk patients Age/comorbidities/PVE/DM Complicated IE (heart failure, shock…) High-risk agents (S.aureus, fungi…), ATB failure TTE/TEE high-risk morphology parameters – risk of embolisation
Slide 18-

Antibiotics • beta-lactam (penicillin, cefalosporin) • glykopeptide (vancomycine) • aminoglykosides (gentamicin) • rifampicin in PVE Fungi – ATB centre expert consult
Slide 19-

Antibiotics • Streptococci: PEN/CEF + GENTA, (VANCO) • Enterococci: like streptococci, PEN resist. common • Staphylococci: MET/OXA + GENTA • Empiric therapy - should focus on S. aureus • HACEK/early PVE/fungi - require expert ATB consult • PVE - prolonged (min. 6w) + RIFAMPIN
Slide 20-

Antibiotics • Usually 4-6 weeks (regardless of surgery) • No fever and decrease in CRP are good markers of th. success, TTE follow-up (< 2weeks) necessary • Cessation of therapy in case of: normal CRP (1w), favourable TTE, no embolisation (2w), absence of focus for potential reinfection
Slide 21-

Surgery progressive heart failure (emergency in shock) signs of ATB th. failure - continuous fever, abscess, vegetation, valve dehiscence… embolization potential (> 10 mm)
Slide 22-

ppt slide no 22 content not found
Slide 23-

PVE • 1% / 1 yr / patient • risk: mechanical similar to biological (later!) • most common manifestation – valve regurgitation • long-term sterilisation rare - surgery likely !!! • early PVE = aggressive pathogens in sewing material, rapidly spreading into surroundings • late PVE = NVE like
Slide 24-

ppt slide no 24 content not found
Slide 25-

PM/ICD IE • IE anywhere on/close to electrodes • S. aureus most likely • Electrode withdrawal necessary (embolisation during withdrawal common, rarely clinically significant)
Slide 26-

ppt slide no 26 content not found
Slide 27-

IVDU • Most commonly Tricuspid valve • S. aureus, pseudomonas, G-, fungi, polymicrobial • Fever, septic pulmonary embolisation (cough, hemoptysis, pulmonary abscesses, …) • Mortality < 10% , but high likelihood of recurrence, surgery common
Slide 28-

Prevention • Restrictive approach • High risk patients only Prosthetic valve implant Previous IE Congenital Heart Disease patients • High-risk procedures (dental)
Slide 29-

ppt slide no 29 content not found
Slide 30-

ppt slide no 30 content not found
Slide 31-

Myocarditis
Slide 32-

Overview Inflammatory disease of the myocardium with a wide range of clinical presentations, from subtle to devastating Usually manifests in otherwise healthy person Wide variety of infectious organisms, autoimmune disorders and exogenous agents Acute phase (0-2wks): direct cytotoxic effect + cell mediated cytotoxicity Chronic phase (>2wks): mainly autoimmune
Slide 33-

Etiology • “Idiopathic” in 50% of cases • Viruses - Enterovirus, Coxsackie A,B, Adenovirus, Parvovirus B19, Influenza, CMV,EBV, HCV, HIV… • Bacterial - streptococci, TBC, diptheria, Borrelia, Chlamydia, Mycoplasma • Fungi – Aspergillus, Candida Protozoa – Trypanosoma cruzii • Drugs - anthracyclines, cocaine • Rheumatic fever • Autoimmune disorders – SLE, Sarcoidosis, Sjögren sy, Churg-Strauss sy, Wegeners granulomatosis, „giant-cell“ myocarditis
Slide 34-

Clinical presentation • flu-like symptomes, arthralgias, malaise, fever pharyngitis, tonsillitis, upper respiratory tract infection • Chest pain, sweats, dyspnea, palpitations • Signs of heart failure, cardiogenic shock • Syncope or sudden cardiac death due to underlying ventricular arrhythmias or AV block)
Slide 35-

Diagnostic workup • Complete blood count, erythrocyte sedimentation rate level, CRP, rheumatologic screening, cardiac biomarkers (TnI, TnT) • Viral antibody titers - rarely indicated, low specificity and delayed rising, no impact on therapeutic decisions • ECG - nonspecific - sinus tachycardia, ST-T changes, AV blocks • Echocardiography (TTE) - to estimate dysfunction and rule-out other causes
Slide 36-

Diagnostic workup • CAG (coronary angiography)- rule-out CAD • MRI (late gadolinium enhancement) - extent of inflammation and cellular edema, nonspecific • EMB (endomyocardial biopsy) - routine use rarely helpful, mandatory in rapidly progressive HF to rule-out giant-cell myocarditis
Slide 37-

ppt slide no 37 content not found
Slide 38-

Treatment Standard HF treatment (ACEi, BB, ARB, diuretics, inotropics,…IABP, LVAD in shock) Avoid physical stress (several months) Routine use of immunosuppression not recommended Immunosuppression used in giant-cell myocarditis or in systemic autoimmune disease (SLE, RA…)
Slide 39-

Follow-up Ongoing, chronic inflammation may cause DCM (dilated cardiomyopathy) and subsequent HF Patients with a history of myocarditis should be monitored at 1-3 months interval initially, with gradual return of physical activity Any evidence of residual cardiac dysfunction should be treated in the same manner as for chronic HF
Slide 40-

Prognosis • Patients who survive fulminant myocarditis generally have good prognosis • Most patients with mild symptoms recover completely without any residual cardiac dysfunction, although up to 30% develop DCM • 90% of patients with giant-cell myocarditis die or undergo Tx in 6 months
Slide 41-

Pericarditis
Slide 42-

Acute pericarditis is an inflammation of the pericardium characterized by chest pain, pericardial friction rub, and serial ECG changes Pain usually precordial or retrosternal with referral to the trapezius ridge, neck, left shoulder, or arm quality is usually pleuritic, range from sharp, dull, aching, burning, or pressing, intensity varies, is worse during inspiration, when lying flat, or during swallowing and with body motion, it may be relieved by leaning forward while seated
Slide 43-

Clinical presentation Intermittent fever dyspnea/tachypnea (!myocarditis, pericarditis, and cardiac tamponade) cough, dysphagia Any form of pericardial inflammation may cause effusion Myocarditis ↔ myopericarditis Pericarditis ↔ perimyocarditis
Slide 44-

Etiology Idiopathic causes - about 50%, likely viral Infectious Viral – enterovirus,echovirus, parvovirus, EBV, HIV… bacterial, TBC, mycotic (Candida) Inflammatory disorders - RA, SLE, scleroderma, rheumatic fever, Reiter sy, dermatomyositis Metabolic – renal failure, hypothyroidism, Cardiovascular disorders - acute MI, Dressler syndrome, Iatrogenic – postpericardiotomic sy, catheterization Neoplasms – adjacent / secondary / paraneoplastic Drugs, Irradiation Trauma, Pneumonia, Pulmonary infarction…
Slide 45-

Diagnostic workup • ECG changes • chest radiograph (enlarged if effusion >250ml) • TTE (effusion), CT (calcification), MRI • Laboratory studies (Complete blood count, ESR, CRP, cardiac TnI/TnT, electrolytes, BUN, creatinine, thyroid hormones + specific (RF...)) • CAG ?
Slide 46-

ppt slide no 46 content not found
Slide 47-

ppt slide no 47 content not found
Slide 48-

Treatment • If specific cause revealed, treat accordingly (ATB) • Idiopathic or viral treated for symptom relief NSAIDs in full dose for 7-14 days (600-800 mg ibuprofen /day), consider PPI as gastric protection Colchicine (recurrence or beyond 14 days, 1 mg/day) Corticosteroids - not for initial therapy, unless specific therapy (autoimmune) or no response to NSAIDs + colchicine • Pericardiocentesis – large effusions, cardiac tamponade
Slide 49-

Treatment • usually when recurrence or large effusions • pericardial window • pericardectomy - in constrictive pericarditis Surgical therapy
Slide 50-

Complications The most common complication of idiopathic acute pericarditis is recurrence, 15 -30 % Constrictive pericarditis Acute and subacute forms of pericarditis may deposit fibrin → pericardial effusion → further pericardial inflammation, chronic fibrotic scarring, calcification, and restricted cardiac filling
Slide 51-

Complications Cardiac tamponade especially in acute pericardial hemorrhage or large chronic malignant effusions accumulation of fluid in the pericardial space resulting in reduced ventricular filling and subsequent hemodynamic compromise medical emergency
Slide 52-

Complications Cardiac tamponade Symptoms vary with the acuteness and underlying cause Dyspnea, tachycardia, tachypnea, hypotension Elevated jugular venous pressure Pulsus paradoxus chest pain, fever, dysphoria
Slide 53-

ppt slide no 53 content not found
Slide 54-

Thank You.
Slide 55-

ppt slide no 55 content not found