This document discusses acquired heart disease, including infective endocarditis and rheumatic heart disease. Infective endocarditis is an inflammation of the heart valves caused by bacteria, viruses or fungi. It is associated with conditions like intravenous drug use or structural heart defects. Rheumatic heart disease results from rheumatic fever, an immune response to a streptococcal infection that damages the heart valves. It presents with manifestations like migratory polyarthritis, heart valve involvement, and Sydenham's chorea. Both require long-term antibiotic treatment and prevention of recurrent infections to avoid further valve damage.

1. Acquired Heart Disease
For Anesthesia II
Abinet Mariyo

2. Outline
• Definition
• Etiology
• Pathogenesis
• Diagnosis and c/f
• Treatment
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3. Infective Endocarditis
• Is an acute and sub acute inflammation of the
endocardium caused by bacteria, virus or fungi.
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4. Etiology
• Viridans type streptococci ( after dental procd.)
• Staphylococcus aureus ( no underlying heart defect)
• Group D enterococci ( lower GI or GU manipulation)
• Others pseudomonas aeruginosa in IVDA
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5. Epidemiology
• Males are commonly affected
• IE is often a complication of congenital or Rheumatic
Heart Disease
• Can occur in children with out any abnormal valves or
cardiac malformation
• In developed countries CHD is commonest
predisposing factor
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6. Pathogenesis
• Patients with CHD where there is a turbulent blood
flow, if there is high pressure gradient across the
defect, turbulent flow Traumatizes the Endothelium,
creates a substrate for deposition of fibrin and
platelets
• Formation of non bacterial thrombotic embolus
which is initiating lesion for IE
• Transient bacteremia there will be colonization of
NBTE by bacteria and Bacterial proliferation occurs
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7. Risk factor
• Intravenous Drug use
• Prosthetic heart valves
• Structural Heart Disease(CHD/RHD)
• Central venous catheter
• Dental, Intestinal or Urinary tract procedure
In 30% a predisposing factor is identified
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8. Clinical Manifestation
• Onset may be acute and severe with HGIF and
prostration
• Prolonged fever without other manifestations
• Common Symptoms are
• Myalgia, arthralgia, headache, nausea and vomiting
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9. Physical Examination
• New/ changing heart murmur
• Splenomegaly
• Signs of Heart Failure
• clubbing
• Classic skin findings develop late in the course of the
disease
• Osler Nodes (tender pea sized intradermal nodules in the pads of
fingers)
• Janeway Leshions (painless small hemorrhagic lesions on palms and soles)
• Splinter Hemorrhages
• This lesions may represent vasculitis prodiced by Ag-Ab Complex
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10. Osler Node
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11. Janeway leshion
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12. Splinter hge
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13. Petechie
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14. Dx Dukes Criteria
• Major
1. Positive Blood cultures( 2 separate culture for usual pathogen, 2
or more for less typical pathogens)
2. Evidence of endocarditis on Echocardiography
• Intracardiac mass on a valve or other site
• Regurgitant flow near a prosthesis
• Abscess
• Partial dehiscence of a prosthetic valves
• New valve regurgitant flow
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15. • Minor
1. Predisposing condition
2. Fever
3. Embolic vascular signs
4. Immune complex phenomena( glomerulonephritis, arthritis, RF,
Osler nodes, Roth spots)
5. A single positive blood culture or serologic evidence of infection
6. Echocardiographic signs not meeting the major criteria
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16. Other minor criteria's
• Clubbing,
• splenomegaly,
• splinter hemorrhages, and
• petechiae,
• elevated ESR,
• elevated CRP,
• microscopic hematuria
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17. • 2 Major
• 1 Major + 3 minor
• 5 minor
Suggest definite IE
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18. Complications
• Cardiac:
• Heart failure
• Myocardial Abscess
• Toxic myocarditis
• Systemic emboli
• Embolic stroke
• Cerebral abscess
• Mycotic aneurism and Hemorrhage
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19. LAB
• Blood Culture
• ESR
• CRP
• CBC( anemia, leukocytosis)
• RF
• U/A ( hematuria)
• CXR
• Echocardiography
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20. Treatment
• Antibiotics
• Vancomycin and Gentamycin until culture result arrives( 4-6 wks)
• If Heart Failure- Diuretics
• Surgical intervention
• Recurrent emboli
• Increasing size of vegetation while receiving Rx
• Failure to sterilize blood after adequate antibiotics
• Severe Aortic/ Mitral valve involvement with intractable HF
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21. Prevention
• Improving dental hygiene
• Careful asepsis during cardiac surgery
• Antimicrobial prophylaxis before dental and other
surgical procedures
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22. Acute Rheumatic Fever
• Is a non suppurative sequelae of GAS(S.pyogenes)
infection.
• 2/3 of patients with Acute rheumatic fever have hx
of URTI several weeks before
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24. Epidemiology
• World wide rheumatic heart disease remains the
most common form of Acquired heart disease in all
age groups
• Historically, ARF was associated with poverty and
overcrowding
• The incidence of both initial attacks and recurrences
of acute rheumatic fever peaks in children 5-15 yr
of age, the age of greatest risk for GAS pharyngitis
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25. Pathogenesis
• Several theories of pathogenesis have been
proposed, notably the cytotoxicity theory and
immunologic theories.
1. Cytotoxicity
• GAS toxin is involved in the pathogenesis of ARF and RHD
• GAS produces streptolysin O enzyme which is cytotoxic to
mammalian cardiac cells
• Unable to explain the latent period.(2-4wk)
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26. 2. Immunologic theory
• The Antigenicity of several GAS antigens and the immunologic
cross reactivity with cardiac antigens ( molecular mimicry)
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27. Diagnosis and clinical manifestation
• Because no clinical or lab finding is pathognomonic
for ARF, JONEs criteria was introduced
• There are 5 Major and 4 minor criteria's and a
requirement of recent GAS infection
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29. Evidence of Recent infection
• Acute rheumatic fever typically develops 2-4 wk after an acute episode of
GAS pharyngitis at a time when clinical findings of pharyngitis are no longer
present and when only 10-20% of patients still harbor GAS in the throat.
• One-third of patients with acute rheumatic fever have no history of an
antecedent pharyngitis.
• Therefore, evidence of an antecedent GAS infection is usually based on
elevated or rising serum antistreptococcal antibody titers
1. ASO9 anti streptolycin O
2. Anti–DNase B,
3. Antihyaluronidase
• The diagnosis of acute rheumatic fever should not be made in those patients
with elevated or increasing streptococcal antibody titers who do not fulfill
the Jones criteria
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30. • There are 3 circumstances in which the diagnosis of
acute rheumatic fever can be made without strict
adherence to the Jones criteria:
1. when chorea occurs as the only major manifestation of
acute rheumatic fever.
2. when indolent carditis is the only manifestation in
patients who first come to medical attention only
months after the apparent onset of acute rheumatic
fever,
3. in a limited number of patients with recurrences of
acute rheumatic fever in particularly high-risk
populations
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31. Migratory Polyarthritis
• Occurs in ~ 70%
• Involves Larger joints(knee, ankle, elbow, wrist)
• Joint become Hot,red tendr and swollen
• Migratory in nature
• Response to salicylates
• Is non deforming
• Earliest manifestation of ARF
• Monoarthritis and poly arthralgia: taken as Major in high
risk populations
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32. Carditis
• ~50-60%
• The most serious manifestation of ARF
• Endocarditis is a universal finding,
• Mostly Isolated Mitral valve or Combined Mitral and Aortic
valve involved
• Isolated aortic of right sided valvular involvement is quite
uncommon
• Valvular insufficiency is characteristic of acute and
convalescent stages of ARF
• Stenotic lesions (AS, MS) occur years after acute illness
• Tachycardia, Murmur, cardiomegaly, HF
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33. Sydenham Chorea 10-15%
• Usually occur as an isolated frequently subtle mov’t
disorder
• Emotional liability, incoordination, poor school
performance, uncontrollable mov’ts and facial grimacing
• Exacerbated by stress and disappear with sleep
• Occasionally unilateral
• The latent period from acute GAS infection to chorea is
usually substantially longer than for arthritis or carditis
and can be months.
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34. • Clinical maneuvers to elicit features of chorea include:
1. milkmaid’s grip (irregular contractions and relaxations
of the muscles of the fingers while squeezing the
examiner’s fingers),
2. spooning and pronation of the hands when the patient’s
arms are extended.
3. wormian darting movements of the tongue upon
protrusion,
4. examination of handwriting to evaluate fine motor
movements.
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35. Erythema Marginatum
• Rare ~1%
• erythematous, serpiginous, macular lesions with pale
centers that are not pruritic
• It occurs primarily on the trunk and extremities, but
not on the face, and
• it can be accentuated by warming the skin.
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36. Subcutaneous Nodules
• Rare <1%
• nodules approximately 1 cm in diameter along the
extensor surfaces of tendons near bony prominences
• There is a correlation between the presence of
these nodules and significant rheumatic heart
disease.
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37. Minor criteria's (5)
Low risk population
• Polyarthralgia(if arthritis is not used as major criteria)
• Fever >= 38.5
• Elevated ESR >=60mm/hr
• Elevated CRP >=3.0mg/dl
High risk
• Monoarthralgia
• Fever >= 38
• Elevated ESR >= 30mm/hr
• Elevated CRP >= 3mg/dl
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• Prolonged PR interval (unless carditis is a major criterion)

38. Treatment
• Antibiotics: regardless of throat culture result
• Amoxicillin PO for 10 days
• Single IM benzathine penicillin
• Anti-inflammatory Therapy:
• Asprin
• corticosteroids
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39. Prevention
• Prevention of both initial and recurrent episodes of
acute rheumatic fever depends on controlling GAS
infections of the upper respiratory tract.
• Primary Prevention:
• Prevention of initial attacks, depends on identification and eradication of
GAS causing acute pharyngitis.
• Secondary Prevention:
• Individuals who have already suffered an attack of acute rheumatic fever
• Are particularly susceptible to recurrences of rheumatic fever with any
subsequent GAS upper respiratory tract infection. Therefore, these
patients should receive continuous antibiotic prophylaxis to prevent
recurrences
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