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Infective Endocarditis
General definitions and epidemiology Pathophysiology Clinical features Treatment

Infective Endocarditis
Mohammed AlAl-Kebsi For 4th year students 2014

Native Valve Endocarditis NVE I.V. drug abuse Prosthetic Valve End (PVE)

Pathogenesis

EPIDEMIOLOGY
Endocarditis
Infective endocarditis (IE) is lethal if not aggressively treated with antibiotics alone or in combination with surgery. The epidemiology of this condition has substantially changed over the past four decades, especially in industrialized countries. (in Yemen, it is worsening). Congenital heart disease and chronic rheumatic heart disease are often associated with the development of such lesions and are lifelong risk factors for IE. Endocarditis usually occurred more frequently in men than in women, with a 2:1 ratio. The median age of patients has gradually increased from 30 to 40 years of age in the early antibiotic era to 47 to 69 years recently (in Yemen, the reality is diffrent).

Definition
Is an inflammation or infection of the endocardium, which is the inner lining of the heart muscle and, most commonly, the heart valves. It is usually caused by bacterial infection, but can be caused by fungus. Febrile illness (but elderly, renal failure and immunocompromised patients) Persistent bacteremia It has characteristic lesion of microbial infection of the endothelial surface of the heart (vegetation)

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Definition
The vegetation
Variable in size Amorphous mass of fibrin & platelets Abundant organisms Few inflammatory cells

Pathogenesis
The heart is made up of three cellular layers: the epicardium (outermost layer), the myocardium (middle, muscular layer), and the endocardium (innermost layer). The endocardium lines all of the chambers and valves of the heart, and its cells are continuous with those of blood vessels leaving the heart.

Pathogenesis
Healthy endothelium is usually resistant to infection, but any pre-existing lesion can favor attachment of circulating bacteria and promote IE . 55-75% of patients with native valve endocarditis (NVE) have underlying valve abnormalities. Cardiac conditions that cause turbulent flow at the endocardial surface (lining of the heart chambers) or across a valve predispose patients to Infective Endocarditis.

Pathogenesis
When the microorganisms gain access to the bloodstream (oral, skin, IV injection) rapidly adhere to valve surfaces, become persistent at the site of adherence, proliferate to cause local damage and vegetation growth, and ultimately disseminate hematogenously with or without emboli. Typically involves the valves
May involve all structures of the heart
Chordae tendinae Sites of shunting Mural lesions

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Pathogenesis
Predisposing etiology In general: general: The most susceptible cardiac abnormalities for IE are:
Rheumatic Congenital Mitral valve prolapse (MVP) i.v. drug abuse

population
Predisposing etiology
Pediatric population
Aortic valve (Bicuspid aortic valve) VSD Tetralogy of Fallot MVP. Post surgical repair (in the site of surgical repair)

Infective Endocarditis
Predisposing etiology
Adult population
Left side IE
Rheumatic valvular disease
common less prevalent in industrialized nations endocarditis occurs most frequently on the mitral valve followed by the aortic valve.

MVP prominent predisposing factor (20% in young women) Congenital heart disease .
Among adults, the common predisposing lesions are patent ductus arteriosus, ventricular septal defect, and bicuspid aortic valve, the latter particularly found among older men (>60 years).

PVE is the most-severe form of IE, and is associated with high mortality that ranges from 20% to >40%.

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Infective Endocarditis
Predisposing etiology
Adult population
Right side IE Intravenous Drug Abuse
Tendency to involve right-sided valves Distribution in clinical series 46 78% tricuspid 24 32% mitral 8 19% aortic Underlying valve normal in 75 93% S. aureus predominant organism (60-70% of tricuspid cases) High concordance of HIV positivity & IE. Patients undergoing hemodialysis.

Dental surgery, Urologic Gynecologic Skin infections

increase the risk of IE, even if there is no pre-existing anatomic valve deformity.

Rheumatic Congenital (MVP) i.v. drug abuse

Organisms
Majority of cases caused by streptococcus, staphylococcus, enterococcus. Gram negative organisms
P. aeruginosa most common HACEK - slow growing, fastidious organisms that may need 3 weeks to grow out of culture
Haemophilus sp. Actinobacillus Cardiobacterium Eikenella Kingella

CLASSIFICATION

Severity (acute, subacute) Type of valve (native, prosthetic) Site of IE (left, right).

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CLASSIFICATION
Severity
Acute
Toxic presentation Progressive valve destruction & metastatic infection developing in days to weeks Most commonly caused by S. aureus

CLASSIFICATION
Types of valve
Native valve endocarditis (NVE), acute and subacute Prosthetic (artificial) valve endocarditis (PVE), early and late after surgery. Intravenous drug abuse (IVDA) endocarditis

Subacute
Mild toxicity Presentation over weeks to months Rarely leads to metastatic infection Most commonly S. viridans or enterococcus

Infective Endocarditis
Site of IE
Left sided IE
acute and subacute Native valve endocarditis (NVE). Prosthetic valve endocarditis (PVE)

Pathophysiology
Clinical manifestations is related to:
Systemic infection. Embolic (bland or septic). Metastatic infective foci. Congestive heart failure. Immune complex- associated lesion.

Right sided IE
Intravenous drug abuse (IVDA) endocarditis) Device related IE (pace-maker)

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Pathophysiology
Local destructive effects
Valvular distortion/destruction/perforation Chordal rupture Perforation/fistula formation Paravalvular abscess Conduction abnormalities Purulent pericarditis Functional valve obstruction

Clinical Features
The interval between the presumed initiating bacteremia and the onset of symptoms of IE is estimated to be less than 2 weeks in more than 80 percent of patients with NVE. Fever most common sign ass. With chills, weakness but may be absent elderly/debilitated pt/CRF/ severe congestive heart failure/ prior antibiotic therapy. (Fever in presence of valvular disease is diagnosed as IE till prove otherwise) shortness of breath, night sweating, loss of appetite, and weight loss. Proximal arthralgias (oligoarticular arthritis ) of the lower extremities. Murmur present in 80 85% Generally indication of underlying lesion Frequently absent in tricuspid IE Changing murmur Spleenomegaly is more common in subacute IE of long duration.

Classical Peripheral Manifestations

Classical Peripheral Manifestations

Splinter or subungual hemorrhages are dark red, linear, or occasionally flame-shaped streaks in the proximal nail bed. Distal lesions at the nail tip are probably caused by trauma. Osler nodes are small, tender subcutaneous nodules in the pulp of the digits, or occasionally more proximal, that persist for hours to several days. Subconjunctival Hemorrhages

Less common today Not seen in tricuspid endocarditis Petechiae most common but not specific for IE.

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Classical Peripheral Manifestations

Janeway lesions are small erythematous or hemorrhagic macular nontender lesions on the palms and soles and are the consequence of septic embolic events. Roth spots, oval retinal hemorrhages with pale centers, are infrequent findings in IE. Neither these nor Osler nodes are pathognomonic for IE.
Clubbing occurs in 10 to 15% of patients.

Systemic Clinical Features

Systemic emboli
Incidence decreases with effective anti-microbial Rx Brain (stroke), pulmonary artery (PE in TV IE), kidney (ARF), spleen (spleenic infarction- tender spleen)

Neurological sequelae
Embolic stroke 15 20% of patients Mycotic aneurysm

Congestive HF
Due to mechanical disruption (perforation- rupture chordae tendine) High mortality without surgical intervention

Renal insufficiency
Immune complex mediated Impaired hemodynamics/drug toxicity Embolization.

Diagnosis

Diagnosis
LABORATORY FINDINGS
Anemia is found in 70 to 90 percent of patients. Anemia worsens with increased duration of illness and thus in acute IE may be absent. In subacute IE, the white blood cell count is usually normal; in contrast, a leukocytosis with increased segmented granulocytes is common in acute IE. The erythrocyte sedimentation rate (ESR) is elevated. Other tests often indicate immune stimulation or inflammation such as rheumatoid factor (RF) in 50%. The urinalysis is often abnormal, even when renal function remains normal. Proteinuria and microscopic hematuria are noted in 50 percent of patients.

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Diagnosis
BLOOD CULTURE
In patients who have not received prior antibiotics, it is likely that 95 to 100 percent of all cultures obtained will be positive and that one of the first two cultures will be positive in at least 95 percent of patients. Prior antibiotic therapy is a major cause of blood culture negative IE, particularly when the causative microorganism is highly antibiotic susceptible.

Diagnosis
OBTAINING BLOOD CULTURE
Three separate sets of blood cultures, each from a separate venipuncture, obtained over 24 hours, are recommended. Each set should include a bottle containing an aerobic medium and one containing anaerobic medium; at least 10 ml of blood should be placed into each bottle. If a clinically stable patient has received an antimicrobial agent during the past several weeks, it is prudent to delay therapy so that repeated cultures can be obtained on successive days.

Echocardiography

Vegetations

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Diagnosis
Published criteria for diagnostic purposes in obscure cases High index of suspicion in patients with predisposing anatomy or behavior Blood cultures Echocardiography
TTE 60% sensitivity TEE 80 95% sensitive

D. Diagnosis
Acute rheumatic fevers. Vasculitis Fever of unknown origin (FUO) Intra-abdominal infections. Septic pulmonary infarction Atrial myxoma. Patient with SLE may develope sterile valvular vegetations, termed libman sacks lesions.

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Goals of Therapy
1. Eradicate infection 2. Definitively treat sequelae of destructive intra-cardiac and extra-cardiac lesions

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Indications for Surgical Treatment of IntraCardiac Complications

Refractory Heart failure. Unstable prosthesis, prosthesis orifice obstructed Uncontrolled infection despite optimal antimicrobial therapy Relapse of PVE after optimal therapy Large vegetation. Abscess formation.

Prevention

Prophylactic regimen targeted against likely organism (SBE prophylaxis)

Strep. viridans oral, respiratory, eosphogeal Enterococcus genitourinary, gastrointestinal S. aureus infected skin, mucosal surfaces

Procedure need SBE prophylaxis

Dental procedures known to produce bleeding Tonsillectomy Surgery involving GI, respiratory mucosa Esophageal dilation Gallbladder surgery Cystoscopy, urethral dilation Urethral catheter if infection present Urinary tract surgery, including prostate

Prevention the underlying lesion

High risk lesions
Prosthetic valves Prior IE Cyanotic congenital heart disease PDA AR, AS, MR,MS with MR VSD Coarctation Surgical systemicsystemic-pulmonary shunts Lesions at highest risk

Intermediate risk
MVP with murmur Pure MS Tricuspid disease Pulmonary stenosis Bicuspid Ao valve with no hemodynamic significance

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Prevention the underlying lesion

Low/no risk
MVP without murmur Trivial valvular regurg. Isolated ASD Implanted device (pacer, ICD) CAD CABG

SBE prophylaxis
Adult Prophylaxis: Dental, Oral, Respiratory, Esophageal Standard Regimen Amoxicillin 2g PO 1h before procedure or Ampicillin 2g IM/IV 30m before procedure Penicillin Allergic Clindamycin 600 mg PO 1h before procedure or 600 mg IV 30m before Cephalexin OR Cefadroxil 2g PO 1 hour before Cefazolin 1.0g IM/IV 30 min before procedure Azithromycin or Clarithromycin 500mg PO 1h before

Adult Genitourinary or Gastrointestinal Procedures

High Risk Patients Standard Regimen Before procedure (30 minutes): Ampicillin 2g IV/IM AND Gentamicin 1.5 mg/kg (MAX 120 mg) IM/IV After procedure (6 hours later) Ampicillin 1g IM/IV OR Amoxicillin 1g PO Penicillin Allergic Complete infusion 30 minutes before procedure Vancomycin 1g IV over 1-2h AND Gentamicin 1.5 mg/kg IV/IM (MAX 120 mg) Moderate Risk Patients Standard Regimen Amoxicillin 2g PO 1h before OR Ampicillin 2g IM/IV 30m before Penicillin Allergic Vancomycin 1g IV over 1-2h, complete 30m before
This wallet card is to be given to patients by their physician. Healthcare professionals, please see back of card for reference to the complete statement.

Name: ____________________________________________ needs protection from BACTERIAL ENDOCARDITIS because of an existing HEART CONDITION Diagnosis: __________________________________________ Prescribed by: _______________________________________ Date: ______________________________________________

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Summary A good doctor is a good observer

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