Infective endocarditis

Olcay ÖZVEREN, M.D.

Definition

Infective endocarditis is characterized by colonization or invasion of the heart valves orthe mural endocardium by a microbe, leading to the formation of bulky,friable vegetations composed of thrombotic debris and organisms, often associated with destruction of the underlying cardiac tissues

A changing epidemiology: Once a disease affecting young adults with previously well-

identified (mostly rheumatic) valve disease, IE is now affecting older patients who more often develop IE as the result of health care-associated procedures, either in patients with no previously known valve disease or in patients with prosthetic valves.

Trials showed an increasing incidence of IE associated with a prosthetic valve, an increase in cases with underlying mitral valve prolapse, and a decrease in those with underlying rheumatic heart disease.

Newer predisposing factors have emerged—valve prostheses, degenerative valve sclerosis, intravenous drug abuse—associated with increased use of invasive procedures at risk for bacteraemia, resulting in health care-associated IE.

3–10 episodes/100 000 person-years. increased dramatically with age. The male:female ratio is 2:1. Positive blood cultures representing 85% of all

IE. Causative microorganisms are most often

staphylococci, streptococci, and enterococci. S. Aureus is the most frequent cause not only of

IE but also of prosthetic valve IE. Conversely, coagulase-negative staphylococci can also cause native valve IE. Especially S. lugdunensis, which frequently has an aggressive clinical course.

Oral (formerly viridans) streptococci species such as S. sanguis, S. mitis, S. salivarius, S. mutans, and Gemella morbillorum. Microorganisms of this group are almost always susceptible to penicillin G.

Infective endocarditis with negative blood cultures because of prior antibiotic treatment.

Infective endocarditis associated withnegative blood cultures They are usually due to fastidious organisms such as …nutritionallyvariant streptococci …fastidious Gram-negative bacilli of the HACEK group: (Haemophilus parainfluenzae, H. aphrophilus, H.

paraphrophilus, H. influenzae, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae, and K. denitrificans), …Brucella…fungi.…Infective endocarditis associated with constantly negative

blood cultures: Coxiella burnetii, Bartonella, Chlamydia Tropheryma whipplei,

Classification and definitions of infective endocarditis

Classification of infective endocarditis

Classification of infective endocarditis

Pathophysiology The normal valve endothelium is resistant to

colonization and infection by circulating bacteria.

mechanical disruption of the endothelium (Endothelial damage may result from mechanical lesions

provoked by turbulent blood flow, electrodes or catheters inflammation, as in rheumatic carditis, or degenerative changes in elderly individuals, which are associated with inflammation, microulcers, and microthrombi)

exposure of underlying extracellular matrix proteins

the production of tissue factor the deposition of fibrin and platelets

-Nonbacterial thrombotic endocarditis (NBTE)-

Microbial pathogens and host defences Classical IE pathogens (S. aureus, Streptococcus

spp., and Enterococcus spp.) share the ability to adhere to damaged valves, trigger local procoagulant activity, and nurture infected vegetations in which they can survive.

surface determinants that mediate adherence to host matrix molecules present (e.g. fibrinogen, fibronectin, platelet proteins)

trigger platelet activation. colonization Gram positive bacteria are resistant to

complement. However, they may be the target of platelet microbicidal proteins (PMPs), which are produced by activated platelets and kill microbes by disturbing their plasma membrane.

Bacteria resistant to PMP-induced killing, THİS is a typical characteristic of IE-causing

pathogens.

Janeway Lesions

1. More specific2. Erythematous, blanching macules 3. Nonpainful4. Located on palms and soles5. Microabscess of the dermis with marked necrosis and inflammatory

infiltrate not involving the epidermis.

Osler’s Nodes

1. More specific2. Painful and erythematous nodules3. Located on pulp of fingers and toes4. immuncomplex

Splinter Hemorrhages

1. Nonspecific2. Nonblanching3. Linear reddish-brown lesions found under the nail bed4. Usually do NOT extend the entire length of the nail 5. vessel damage from swelling of the blood vessels (vasculitis) or

tiny clots that damage the small capillaries (microemboli).

Petechiae

1.Nonspecific2.Often located on extremities

or mucous membranes

Roth Spots

septic embolization, leukemia, lupus erythematosus, or pernicious anemia.

Imaging

Chest x-ray Look for multiple focal infiltrates and

calcification of heart valves EKG

Rarely diagnostic Look for evidence of ischemia,

conduction delay, and arrhythmias Echocardiography

Complications

1.1. Congestive heart failureCongestive heart failure• Most common complication• Main indication to surgical treatment• ~60% of IE patients

2.2. Uncontrolled infectionUncontrolled infection• Persisting infection • Perivalvular extension in infective

endocarditis3.3. Systemic embolismSystemic embolism

• Brain, spleen and lungs• 30% of IE patients• May be the first symptom

Complications

5.5. Neurologic eventsNeurologic events

6.6. Acute renal failureAcute renal failure

7.7. Rheumatic problemsRheumatic problems

8.8. MyocarditisMyocarditis

Cardiac conditions at highest risk of infective endocarditis for which prophylaxis is recommended when a high risk procedure is performed

Recommendations for prophylaxis of infective endocarditis

Definition Current Diagnosis 07

An acute systemic immune disease that may develop after an infection with Group A beta- hemolytic Streptococcal infection of the pharynx.

This disease can affect the HEART, JOINTS, SKIN, SUBCUTANEOUS TISSUE, BRAIN, RESPIRATORY SYSTEM, VESSELS, SEROSAL MEMBRANES, TENDONS AND FASCIAL SHEATHS

General Consideration

Pathology

PATHOLOGY

The Aschoff bodies comprises a localised area of inflammation having a central deposit of amorphous fibrinoid material surrounded by an inflammatory infiltrate of mesenchymal cells known as Anitschkow giant cells or “caterpillar cells” (because the chromatin is distributed in the centre of the nucleus in the forrm of a slender wavy ribbon that resemles the attenuated body with innumerable fine leg like projections )

and an occasional multinucleated Aschoff giant cell with”owl eyed” nucleoli

Fully developed Aschoff bodies are pathognomonic of RF

Aschoff bodies proceed thru 3 phases- exudative, proliferative and healed

The heart has been sectioned to reveal the mitral valve as seen from above in the left atrium. The mitral valve demonstrates the typical "fish mouth" shape with chronic rheumatic scarring. Mitral valve is most often affected with rheumatic heart disease, followed by mitral and aortic together, then aortic alone, then mitral, aortic, and tricuspid together.

                                 

Microscopically, acute rheumatic carditis is marked by a peculiar form of granulomatous inflammation with so-called "Aschoff nodules" seen best in myocardium. These are centered in interstitium around vessels as shown here. The myocarditis may be severe enough to cause congestive heart failure.

Here is an Aschoff nodule at high magnification. The most characteristic component is the Aschoff giant cell. Several appear here as large cells with two or more nuclei that have prominent nucleoli. Scattered inflammatory cells accompany them and can be mononuclears or occasionally neutrophils.

                                 

Another peculiar cell seen with acute rheumatic carditis is the Anitschkow myocyte. This is a long, thin cell with an elongated nucleus.

MODIFIED JONES’ CRITERIA

MAJOR: Polyarthritis Carditis Chorea Subcutaneous nodules Erythema marginatum

MINOR CRITERIAClinical Fever Polyarthralgia h/o previous ARF or Rheum. heart diseaseLab Reversible prolongation of PR interval Inc ESR Inc C Reactive Protein + throat culture Or rapid streptococcal

antigen test Inc ASO titre

Laboratory Findings

Supporting evidence of Streptecoccal infection

Rapid antigen detecting test

REQUIRED FOR DIAGNOSIS

Two major criteria OR One major and two minor criteria

Exceptions to Jones Criteria

POLYARTHRITIS Migratory – flitting and fleeting Involves large joints sequentially Polyarthritis- in adults only a single joint

may be affected Lasts 1-5 weeks Occurs in 75% or patients Subsides without residual deformity Dramatic response of arthritis to

therapeutic doses of aspirin or NSAIDs

CARDITIS Most likely in children and adolescents Occurs in 1/3 of cases Any of the following signs suggest the presence of carditis

1. Endocardial-

- MR or AR murmurs indicative of dilatation of valve ring with or without associated valvulitis

-Short mid-diastolic murmur (Carey-Coombs) may be present

- Changing quality of heart sounds

2. Myocardial

- Tachycardia even at rest. Arrhythmias or ectopic beats

- Cardiomegaly- on physical exam, CXR or ECHO

- Congestive cardiac failure – right or left sided

3. Pericardial

- Pericarditis

- Pericardial effusion

ECG Changes

- Changing contour of P waves

- Inversion of T waves

- Prolongation of PR interval

Maybe self limiting or may lead to slowly progressive valvular deformity

Mitral valve attacked in 75% cases, aortic in 30% ( but rarely as the sole valve), tricuspid and pulmonary in < 5% cases

SYDENHAM’S CHOREA Involuntary choreo- athetoid movements

primarily of the face, tongue, and upper extremities,detoriation of hand writing,emotional lability ,grimacing of face

Maybe sole manifestation- in 50% of cases no other signs of RF

Girls more frequenty affected Rare in adults Lease common(<3%) but most diagnostic of

the manifestations of RF May appear even 6-12 years after the acute

phase of RF

Erythema Marginatum

.

Subcutaneous Nodule

Imaging

DIFFERENTIAL DIAGNOSIS

Rheumatoid arthritis Osteomyelitis Endocarditis Chronic meningiococcemia SLE Lyme disease Sickle cell disease Surgical abdomen

TREATMENT

PHARYNGITISBenzathene penicillin 1.2 million units ( 50,000 units/kg to a max of 1.2

million units) is injected IM once orInj Procaine penicillin 600,000 units once daily for 10 daysErythromycin can be substituted ( 40mg/kg/day)CARDITIS Bed rest – until temp, ESR, resting pulse rate and ECG have all returned

to normal Prednisone if there is CCF or cardiomegalyPOLYARTHRITIS Anti inflammatory agent - Aspirin markedly reduces fever, joint pain and

swelling No effect on the natural course of the disease 100mg / kg/day in 4-6 divided doses. Can be reduced to 75mg/Kg/day

once there is a response . Given for 4-6 weeks Toxicity includes- tinnitus, vomiting and GI bleeding. When response to aspirin is inadequate a short course of prednisone (1

mg/kg/day) orally daily usually causes rapid improvement of joint symptoms. It is tapered over 2 weeks. Add aspirin when tapering begins.

Treatment Strategy

Other alternative drugs used

Anti inflamatory treatment

Rheumatic carditis without failure

Rheumatic carditis without failure

Management of complications