Ineffective endocarditis and rheumatic fever

Question 1

What is rheumatic fever?

Answer 1

• A multisystem disease which occurs after a group A streptococcal infection
• Affects heart, skin, joints and central nervous system

Question 2

Describe the aetiopathogenesis of rheumatic fever.

Answer 2

Occurs after Group A, beta haemolytic streptococcal infection.

2-6 week layent period before onset of rheumatic fever.

Question 3

What are the risk factors for rheumatic fever?

Answer 3

• Patients from low socio-economic groups
• Overcrowded conditions
• HLA DR4 positive

Question 4

How does rheumatic fever occur?

Answer 4

Occurs after repeated oropharyngeal streptococcal infections causing an exaggerated B lymphocyte response.

Streptococcal antigens cross react with connective tissue

Question 5

What might people with rheumatic fever develop?

Answer 5

1. Vasculitis affecting the connective tissue (inflammation of vessel walls)
2. Aschoff’s body, consisting of an aggregate of large cells with polymorphs & basophils around a vascular fibrinoid core
3. Pancarditis with the endocardium being the most severely involved (inflammation of all walls of the heart)

Chronic rheumatic fever may develop in 50% of patients with acute rheumatic fever

1% mortality in patients’ with carditis

Question 6

How do you make a diagnosis of rheumatic fever?

Answer 6

-Duckett-Jones criteria

-Presence of 2 major & 1 minor criteria indicates high probability of rheumatic fever

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Question 7

What is the prevalence of polyarthritis after the strep sore throat & what does it affect?

Answer 7

Polyarthritis occurs in 80-90% of patients but the arthritis is migratory & lasts for 4-6 weeks

It mainly affects the large joints such as the hip, knee, ankle, elbow & shoulder

The pain may last for a week in any particular joint

Question 8

Describe carditis in rheumatic fever. (MAJOR)

Answer 8

occurs in 40-50% of patients

Happens 2 weeks after polyarthiritis and involves all the cardiac tissue

Lasts 3-6 months

Clinical features vary, it may be asymptomatic or may be present with congestive cardiac failure.

Asymptomatic cases are usually only recognised after the presentation of other clinical signs or cardiomegaly on the chest X-Ray

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Question 9

Describe pericarditis in rheumatic fever. (MAJOR)

Answer 9

Occurs in 5-10% of patients

Inflammation of cardiac pericardium

Presents with fluid in the pericardial space and may give rise to an intermittent pericardial rub

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Question 10

Describe myocarditis in rheumatic fever. (MAJOR)

Answer 10

• All of myocardium may be involved
• Patients present with left ventricular failure which may lead to right ventricular failure and subsequent congestive cardiac failure

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Question 11

Describe endocarditis in rheumatic fever. (MAJOR)

Answer 11

• inflammation of inner lining of the heart chambers

-Mitral valve is most commonly affected

-May occur alone or in association with the aortic valve failure

-Mitral + aortic valve disease = fulminant (associated with high mortality rate)
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Question 12

Describe chorea in rheumatic fever. (MAJOR)

Answer 12

• Late symptom, May occur 4 to 6 months after the other features of rheumatic fever
• Involuntary movement of face and limbs

-Disappears during sleep

-occurs in 10% of patients

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Question 13

Describe subcutaneous nodules in rheumatic fever. (MAJOR)

Answer 13

• Subcutaneous nodules = rare
  -Small (up to 0.5cm) are non- tender, mobile and firm
• Occur over bony prominence

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Question 14

Describe erythema nodusum in rheumatic fever. (MAJOR)

Answer 14

• May also occur over the shins
• Larger and more painful than subcutaneous nodules

-Deep pink/Red

-Nodules are tender on palpating

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Question 15

Describe erythema marginatum in rheumatic fever:

Answer 15

• Occurs in 65% of patients
• Painless and non-pruritic rash (not itchy)

-It has a serpinginous edge with a fading centre and spreads over the trunk and limbs

Question 16

What is infective endocarditis (IE)?

Answer 16

Infection of the endocardial surface (inner lining) of heart or valves

Usually bacterial, but occasionally can be fungale

Question 17

What is the morbidity & mortality rate for IE?

Answer 17

Significant (20-30%)

Question 18

Why could incidence of IE be possibly rising?

Answer 18

Increasing no. of elderly ppl (& hence abnormal/prosthetic valves)

Increasing no. of invasive procedures, both diagnostic & therapeutic

Increased no. of children with CHD (congenital heart disease) survive

Increase in IV drug abuse

Question 19

What is the annual incidence of IE in the UK?

Answer 19

6-7 per 100,000 (possibly rising?)

Question 20

What is endocarditis usually a consequence of? (2 factors)

Answer 20

• Abnormal cardiac endothelium facilitating bacterial adherence and growth

-Presence of organisms in the blood

Question 21

Describe the aetiopathogenesis of IE.

Answer 21

1. Abnormal endothelium = creates non-laminar blood flow, promoting fibrin and platelet deposition
2. Due to fibrin and platelet deposition, Small thrombi develop and allow organisms to adhere and grow

• Leads to characteristic infected vegetation

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Question 22

What do a growing number of patients with IE have?

Answer 22

No definable underlying cardiac lesion

e.g. patients over 65 with minor degenerative lesions or IV drug users with periodic introductions of foreign material who have undetectable lesions serving as a nidus

Question 23

What are the primary microorganisms involved in IE?

Answer 23

Streptococci (63%)

Viridans group (50%)

Staphylococci (26%)

Fungi (4%)

Question 24

In what percentage of IE patients is a blood culture negative and why?

Answer 24

-5-10%, possibly due to previous antibiotic therapy

-Fastidious organisms (organisms that are complex and require specific nutritional requirements) that fail to grow in normal blood culture

Question 25

What are the clinical features of IE?

Answer 25

EARLY : Fever, sweats, loss of appetite, weight loss, malaise

LATE : splenomegaly (enlargement of spleen), clubbing (bulbous enlargement of end of finger), anaemia

SIGNS OF HEART DISEASE :
-Development of a new murmur
-Change to an existing murmur
-Heart failure

SIGNS OF EMBOLISM :
-septic arthritis, osteomyelitis, splenic abscess
-CNS - meningitis, miliary brain abscess, TIA, stroke

IMMUNE COMPLEX :
-Skin - Osler’s nodes , Splinter haemorrhage
-Renal - haematuria
-Eyes - Roth’s spots

Question 26

what kind of lesions can infective endocarditis cause?

Answer 26

Osler Node and Janeway Lesions

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Question 27

What investigations would you carry out in a patient with suspected IE?

Answer 27

1. Urine testing ( looking for microscopic haematuria)
2. Blood investigations:
   -FBC - Raised white cell count (leukocytosis). Normochromic normocytic anaemia
   -ESR/CRP Raised
   -LFT mild disturbance, alkaline phosphatase raised
   -Serum Immunoglobulins – Raised
   -Complement and C3 Decreased

3.Chest radiograph (Cardiomegaly and signs of heart failure)

4.Electrocardiogram

5. ECG

Question 28

What treatment options are possible for patients with IE?

Answer 28

Drug therapy
Surgery

Question 29

explain the Parenteral route for IE?

Answer 29

Pharmacotherapy:

Endocarditis is treated with bactericidal antibiotics chosen on the basis of blood culture and antibiotic sensitivity assessment.

The treatment should continue for 4-6 weeks and at least the first two weeks should be parenteral.

Question 30

When would IE be treated with surgery?

Answer 30

SURGERY
There are several situations when surgery is indicated:
1. extensive damage to a valve
2. infection of prosthetic material
3. worsening renal failure
4. persistent infection but failure to culture an organism
5. embolisation
6. large vegetations

Question 31

When is the prognosis of IE worse?

Answer 31

Mortality rate is 15-30%

Prognosis worse when:

1. organism cannot be identified
2. cardiac failure is present
3. infection occurs on a prosthetic valve
4. microorganisms found are resistant to therapy

Question 32

What are the NICE guidelines for prophylaxis against IE?

Answer 32

• This is to reduce the risk of antibiotic resistance

Prophylaxis against infective endocarditis. Antibiotic prophylaxis against infective endocarditis is not recommended routinely:

for people undergoing dental procedures

for people undergoing non-dental procedures at the following sites
upper and lower gastrointestinal tract

genitourinary tract; this includes urological, gynaecological and obstetric procedures, and childbirth

upper and lower respiratory tract; this includes ear, nose and throat procedures and bronchoscopy

Chlorhexidine mouthwash should not be offered as prophylaxis against infective endocarditis to people at risk of infective endocarditis undergoing dental procedures.

Question 33

What should healthcare professionals offer people with increased risk of IE?

Answer 33

Adults and children with structural cardiac defects at risk of developing infective endocarditis

Acquired valvular heart disease with stenosis or regurgitation

Hypertrophic cardiomyopathy

Previous infective endocarditis

Structural congenital heart disease, including surgically corrected or palliated structural conditions, but excluding isolated atrial septal defect, fully repaired ventricular septal defect or fully repaired patent ductus arteriosus, and closure devices that are judged to be endothelialised

Valve replacement.