Ineffective endocarditis and rheumatic fever Flashcards
What is rheumatic fever?
- A multisystem disease which occurs after a group A streptococcal infection
- Affects heart, skin, joints and central nervous system
Describe the aetiopathogenesis of rheumatic fever.
Occurs after Group A, beta haemolytic streptococcal infection.
2-6 week layent period before onset of rheumatic fever.
What are the risk factors for rheumatic fever?
- Patients from low socio-economic groups
- Overcrowded conditions
- HLA DR4 positive
How does rheumatic fever occur?
Occurs after repeated oropharyngeal streptococcal infections causing an exaggerated B lymphocyte response.
Streptococcal antigens cross react with connective tissue
What might people with rheumatic fever develop?
- Vasculitis affecting the connective tissue (inflammation of vessel walls)
- Aschoff’s body, consisting of an aggregate of large cells with polymorphs & basophils around a vascular fibrinoid core
- 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
How do you make a diagnosis of rheumatic fever?
-Duckett-Jones criteria
-Presence of 2 major & 1 minor criteria indicates high probability of rheumatic fever
slide 7
What is the prevalence of polyarthritis after the strep sore throat & what does it affect?
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
Describe carditis in rheumatic fever. (MAJOR)
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
slide 10
Describe pericarditis in rheumatic fever. (MAJOR)
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
slide 11
Describe myocarditis in rheumatic fever. (MAJOR)
- All of myocardium may be involved
- Patients present with left ventricular failure which may lead to right ventricular failure and subsequent congestive cardiac failure
slide 12
Describe endocarditis in rheumatic fever. (MAJOR)
- 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)
slide 13
Describe chorea in rheumatic fever. (MAJOR)
- 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
slide 14
Describe subcutaneous nodules in rheumatic fever. (MAJOR)
- Subcutaneous nodules = rare
-Small (up to 0.5cm) are non- tender, mobile and firm - Occur over bony prominence
slide 15
Describe erythema nodusum in rheumatic fever. (MAJOR)
- May also occur over the shins
- Larger and more painful than subcutaneous nodules
-Deep pink/Red
-Nodules are tender on palpating
slide 15
Describe erythema marginatum in rheumatic fever:
- 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
What is infective endocarditis (IE)?
Infection of the endocardial surface (inner lining) of heart or valves
Usually bacterial, but occasionally can be fungale
What is the morbidity & mortality rate for IE?
Significant (20-30%)
Why could incidence of IE be possibly rising?
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
What is the annual incidence of IE in the UK?
6-7 per 100,000 (possibly rising?)
What is endocarditis usually a consequence of? (2 factors)
- Abnormal cardiac endothelium facilitating bacterial adherence and growth
-Presence of organisms in the blood
Describe the aetiopathogenesis of IE.
- Abnormal endothelium = creates non-laminar blood flow, promoting fibrin and platelet deposition
- Due to fibrin and platelet deposition, Small thrombi develop and allow organisms to adhere and grow
- Leads to characteristic infected vegetation
slide 22
What do a growing number of patients with IE have?
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
What are the primary microorganisms involved in IE?
Streptococci (63%)
Viridans group (50%)
Staphylococci (26%)
Fungi (4%)
In what percentage of IE patients is a blood culture negative and why?
-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
What are the clinical features of IE?
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
what kind of lesions can infective endocarditis cause?
Osler Node and Janeway Lesions
slide 27
What investigations would you carry out in a patient with suspected IE?
- Urine testing ( looking for microscopic haematuria)
- 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
- ECG
What treatment options are possible for patients with IE?
Drug therapy
Surgery
explain the Parenteral route for IE?
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.
When would IE be treated with surgery?
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
When is the prognosis of IE worse?
Mortality rate is 15-30%
Prognosis worse when:
- organism cannot be identified
- cardiac failure is present
- infection occurs on a prosthetic valve
- microorganisms found are resistant to therapy
What are the NICE guidelines for prophylaxis against IE?
- 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.
What should healthcare professionals offer people with increased risk of IE?
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.
