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Infective Endocarditis

Mohammed AlMohammed Al--KebsiKebsi

For 4th year students

2014

Infective Endocarditis

• General definitions and

epidemiology

– Native Valve Endocarditis NVE

– I.V. drug abuse

– Prosthetic Valve End (PVE)

• Pathogenesis

• Pathophysiology

• Clinical features

• Treatment

EPIDEMIOLOGY

• 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

Endocarditis

• Is an inflammation or infection of the endocardium,which is the inner lining of the heart muscle and, mostcommonly, the heart valves. It is usually caused bybacterial infection, but can be caused by fungus.

• Febrile illness (but elderly, renal failure andimmunocompromised patients)

• Persistent bacteremia

• It has characteristic lesion of microbial infection of theendothelial surface of the heart (vegetation)

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Definition

• Variable in size

• Amorphous mass of fibrin & platelets

• Abundant organisms

• Few inflammatory cells

The vegetation • 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

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 blood-

stream (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

InIn generalgeneral::

• The most susceptible cardiac abnormalities for

IE are:

• Rheumatic

• Congenital

• Mitral valve prolapse (MVP)

• i.v. drug abuse

Predisposing etiology

population

• Pediatric population• Aortic valve (Bicuspid aortic valve)

• VSD

• Tetralogy of Fallot

• MVP.

• Post surgical repair (in the site of surgical repair)

Predisposing etiology

Infective Endocarditis

• 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%.

Predisposing etiology

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Infective Endocarditis

• 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.

Predisposing etiology

• Rheumatic

• Congenital

• (MVP)

• i.v. drug abuse

• Dental surgery,

• Urologic

• Gynecologic

• Skin infections

increase the risk of IE,

even if there is no

pre-existing anatomic

valve deformity.

XX

X

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

• Subacute

– Mild toxicity

– Presentation over weeks to months

– Rarely leads to metastatic infection

– Most commonly S. viridans or enterococcus

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

Infective Endocarditis

Site of IE

• Left sided IE

– acute and subacute

– Native valve endocarditis (NVE).

– Prosthetic valve endocarditis (PVE)

• Right sided IE

– Intravenous drug abuse (IVDA) endocarditis)

– Device related IE (pace-maker)

Pathophysiology

• Clinical manifestations is related to:

– Systemic infection.

– Embolic (bland or septic).

– Metastatic infective foci.

– Congestive heart failure.

– Immune complex- associated lesion.

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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 FeaturesThe 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

• Less common today

• Not seen in tricuspid endocarditis

• Petechiae most common but not specific for IE.

• 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

Classical Peripheral Manifestations

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• 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.

Classical Peripheral Manifestations 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.

DiagnosisDiagnosis

• 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.

LABORATORY FINDINGS

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Diagnosis

• 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.

BLOOD CULTUREDiagnosis

• 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.

OBTAINING BLOOD CULTURE

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 Intra-

Cardiac 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 valvesProsthetic valves

–– Prior IEPrior IE

–– Cyanotic congenital heart Cyanotic congenital heart

diseasedisease

–– PDAPDA

–– AR, AS, MR,MS with MRAR, AS, MR,MS with MR

–– VSDVSD

–– CoarctationCoarctation

–– Surgical systemicSurgical systemic--pulmonary pulmonary

shuntsshunts

• Intermediate risk

–– MVP with murmurMVP with murmur

–– Pure MSPure MS

–– Tricuspid diseaseTricuspid disease

–– Pulmonary Pulmonary stenosisstenosis

–– Bicuspid Bicuspid AoAo valve with no valve with no

hemodynamic significancehemodynamic significance

Lesions at highest risk

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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, EsophagealStandard 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 ProceduresHigh 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: ____________________________________________ Name: ____________________________________________

needs protection from needs protection from

BACTERIAL ENDOCARDITISBACTERIAL ENDOCARDITIS

because of an existing because of an existing

HEART CONDITIONHEART CONDITION

Diagnosis: __________________________________________ Diagnosis: __________________________________________

Prescribed by: _______________________________________Prescribed by: _______________________________________

Date: ______________________________________________ Date: ______________________________________________

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Summary

A good doctor is a good observer