Infective Endocarditis and Rheumatic Fever Flashcards

1
Q

Definition of rheumatic fever and what does it affect

A
  • Multisystem disease which occurs after a group A streptococcal infection
  • Affects heart (50% of cases), skin, joints and CNS
  • Inflammatory disease that develops 2-6 weeks after a streptococcal throat infection
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2
Q

Epidemiology of RF

A
  • Often between 5-15 yo

- Most commonly in Iran

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3
Q

Aetiopathogenesis, incubation period and risk factors of RF

A
  • Group A, B haemolytic streptococci
  • Latent period of 2-6 weeks before onsent
  • Streptococcal causes an exaggerated B lymphocyte response
  • Type II Hypersensitivity
  • Streptococcal antigens cross react with connective tissue (molecular mimicry)
  • Bacterial sugar component shares antigenic homology with glycoproteins found in the connective tissue in the human heart valves
  • Pathologic process causing vaculitis affecting the connective tissue
  • Aschoff’s body is the pathologic lesion and consists of an aggregate of large cells with polymorphs and basophils around a vascular fibrinoid core
  • Cardiac lesion characterised by a pancarditis with the endocardium being the most severely involved

-Risk factors include patients from low socio-economic groups, overcrowded conditions and HLA-DDR4 positive

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4
Q

Clinical Features of RF

A

According the the Duckett-Jones Criteria:

-Major Criteria:
Carditis (inflammation of any part of the heart- my, peri or end)
Polyarthritis (arthritis affecting many joints)
Erythema marginatum (red patch rash with a pale centre and a red outer area)
Subcutaneous nodule (nodule below the skin)
Chorea (involuntary movements)

-Minor Criteria:
Fever
Arthralgia (pain in a joint)
Previous rheumatic fever
Raised acute phase proteins such as CRP, ESR and Ferritin 
Prolonged P-R interval on the ECG
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5
Q

Diagnosis of RF

A

Using the Ducket-Jones Criteria, 2 major and 1 minor indicates a high probability of RF

Major:

  • Carditis (inflammation of any part of the heart including myocardium, pericardium or endocardium)
  • Polyarthritis (arthritis of multiple joints)
  • Subcutaneous nodule
  • Erythema marginatum (red patch rash with a pale centre but red surrounding it)
  • Chorea (uncontrolled movements)

Minor:

  • Lab Findings (CRP, ESR and Ferritin Levels)
  • Increase PR interval
  • Previous Rheumatic Fever
  • Fever
  • Arthralgia (pain in the joints)
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6
Q

Carditis definition, importance, clinical features

A
  • Occurs in 50% of RF patients and lasts between 3-6 months
  • Occurs 2 weeks after polyarthritis and involves all the cardiac tissue
  • Pancarditis: inflammation of the entire heart
  • May be asymptomatic or present with congestive cardiac failure
  • Increasing breathlessness, palpatations which may be intermittent and/or chest pain
  • Morbidity and mortality is associated with congestive cardiac failure

-Asymtpmatic cases usually only recognised after presentation of other clinical signs or cardiomegaly on CXR (abnormal enlargement of the heart)

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7
Q

Types of carditis and explanation of how RF affects each

A

-Myocarditis
Involves the myocardium (muscular tissue of the heart)
Clinical consequences are usually due to left and right ventricular involvement
Patients may present with left ventricular failure which may lead to right ventricular failure and subsequent congestive cardiac failure

-Endocarditis:
Inflammation of the inner heart lining and valves
Mitral Valve (Left atrium to left ventricle) most commonly affected. Either occurs alone or in association with the aortic valve failure (Left Ventricle to aorta)
When mitral and aortic valve disease occurs together the disease becomes fulminant and is associated with a high mortality rate
Valvulitis involves nodules on the mitral and aortic valves resulting in murmurs which may change
Mitral valve involvement results in Carey Coombs murmur which is a soft diastolic murmur which is a soft diastolic murmur

-Pericarditis
Inflammation of the cardiac pericardium
Presents with fluid in the pericardial space and may give rise to an intermittant percardial rub

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8
Q

Mitral Valve murmur name and type

A
  • Carey Coombs Murmur

- Soft, Diastolic murmur

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9
Q

Polyarthritis significance, how long, clinical features

A
  • Often first clinical manifestation after streptococcal sore throat
  • 80-90% of patients
  • Arthritis is migratory and lasts for 4-6 weeks
  • Affects large joints such as knee, ankle, elbow hip and shoulder
  • Onset of pain is sudden and associated with one or more joins
  • Accompanies with swelling
  • Pain may last for a week
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10
Q

Chorea, another name, how common and when, clinical features

A
  • Syndenhams Chorea or St Vitus Dance
  • 10% of patients
  • Late clinical manifestation, often 5 months after other manifestations
  • Involuntary movements of the face and limbs nut disappears during sleep
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11
Q

Subcutaneous nodules how common, clinical features and other types

A
  • Rare
  • Small that are non-tender, mobile and firm
  • Occur over bony prominences eg. elbows

-Erythema nodosum may also occur over the shins
Larger than subcutaneous nodules and are painful
Appear as deep pink/red nodules and are tender on palpation

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12
Q

Erythema Marginatum how common, clinical features

A
  • 65% of pts
  • Invariably seen in association with carditis
  • Rash is painless and non-pruritic
  • Not a well defined boundary, with a fading centre
  • Spreads over the trunk and limbs
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13
Q

Complications of RF

A

-Either a predisposition of infective endocarditis or endocarditis itself

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14
Q

Definition of infective endocarditis

A
  • Infection of the endocardial surface of the heart
  • Includes the inner lying and the valves
  • Usually bacterial, occasionally fungal
  • Morbidity and mortality (20-30%)
  • Maybe an acute, fulminating infection, but more commonly runs an insidious course known as subacute bacterial endocarditis (SBE)
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15
Q

Aetiology of IE

A

-Endocarditis usually a consequence of 2 factors:
Abnormal cardiac endothelium facilitating bacterial adherence and growth
Presence of organisms in the blood

  • Abnormal endothelium is usually a result of a valvular lesion, which creates non-laminar, turbulent flow, promoting fibrin and plately deposition
  • Small thrombi allow organisms to adhere and grow
  • Leads to characteristic infected vegetation
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16
Q

Epidemiology of IE and possible explanation

A

-Rising possibly as a result of:
Increased numbers of elderly (and hence abnormal, prosthetic valves)
Increased numbers of invasive procedures both diagnostic and therapeutic
Increased number of children with Coronary HD surviving
Increase in IV drug abuse, allowing bacteria and other organisms into the blood

17
Q

Clinical Spectrum of IE

A

-Growing proportion of pts have no definable underlying cardiac lesion
Pts over 65 with minor degenerative lesions
IV drug addicts with periodic introduction of foreign material, but have undetectable lesions serving as nidus

18
Q

Organisms involved in pathogenesis of IE and significance

A
  • Streptococci 60%
  • Viridans group 50%
  • Staphylococci 26%
  • Fungi 4%

-Commonly found in the oral cavity!

  • Culture negative in 5-10%, possibly due to previous antibiotic therapy
  • Fastidious organisms that fail to grow in normal blood cultures
  • Difficult to treat these pts because no identifiable cause
19
Q

Pathogenesis of IE

A

-Endothelial trauma due to:
Immune complex deposition eg. Rheumatic heart disease, SLE
Local stresses related to blood turbulence with jet streams and eddy currents

  • Non-laminar blood flow, promoting fibrin and platelet deposition
  • Endothelial damage exposes the connective tissue which leads to platelet aggregation and deposition of fibrin and platelets to form sterile vegetations
  • Sterile vegetations serve as nidus for microorganisms to adhere and colonise
  • Certian pathogens favoured as they adhere readily or elude host immune system
  • Further deposition of fibrin and platelets protects the bacterial
  • Bacterial multiply and further platelet deposition produces vegetations
20
Q

Clinical Features of IE

A

-Signs of Infection
Early: fever, sweats, anorexia, weight loss, malaise
Late: splenomegaly, clubbing, anaemia

-Signs of heart disease
Development of a new murmur
Change in existing murmur
Heart Failure

-Signs of embolism
Septic arthritis, osteomyelitis, splenic abscess
CNS- meningitis, miliary brain abscess, TIA

-Immune Complex
Skin- Osler’s nodes, splinter haemorrhage
Renal- haematuria
Eyes- Roth’s spots

21
Q

Common cutanous manifestations of IE

A
  • Osler Node: painful, tender, nodular area often in the thumbs
  • Janeway lesions: non tender
22
Q

Investigations for IE

A

-Urine Testing
Look for microscopic haematuria

-Blood Cultures
Positive in 75% of cases

-Bloods
FBC
Raised white cell count (leukocytosis)
Normochronic normocytic anaemia
Raised ESR
LFT- increase in alkaline phosphatase
Serum immunoglobulins increase but complement and C3 decrease 

-CXR
Cardiomegaly and signs of heart failure

  • ECG
  • Echocardiogram
23
Q

Treatment of IE

A

-Drug Therapy
Dentistry should occur before starting therapy or 4 weeks after tx
Endocarditis is treated with bactericidal antibiotics chosen on the basis of blood culture and antibiotic sensitivity assesement
Tx should continue for 4-6 weeks and the first 2 weeks should be IV antibiotics

-Surgery maybe indicated if:
Extensive damage to a valve
Infection of a prosthetic material 
Worsening renal failure 
Persistent infection but failure to culture an organism 
Embolisation 
Large vegetations 

Infection should always be eliminated first

24
Q

Prognosis of IE get worse if

A
-Worse when
Organism cannot be identified 
Cardiac failure present 
Infection on prosthetic valve
Microorganisms are found resistant to therapy
25
Q

Prophylaxis for IE?

A
  • Previously antibiotic prophylxis was required to protect those at risk of developing IE
  • At risk group included prosthetic heart valves, previous IE, congenital heart disease, mitral valve prolapse
  • But not anymore
  • Only give propylaxis to very high risk patients with previous history
26
Q

Dental Relevance of IE

A
  • Take care with all dental procedures associated with significant bacteraemia
  • Careful treatment planning is required to minimise clinical sessions
  • Previously antibiotic prophylxis was required to protect those at risk of developing IE
  • At risk group included prosthetic heart valves, previous IE, congenital heart disease, mitral valve prolapse
  • But not anymore
  • Only give propylaxis to very high risk patients with previous history
  • Discuss with cardiologist if unsure