Arf/ Rhd/ IE Flashcards

1
Q

Acute rheumatic fever?

A

A nonsuppurative sequela that occurs two to four weeks following
group A Streptococcus(GAS) pharyngitis( by S.pyogens))

Usually affects children and young adults between the ages of 5 and
17 years.

It is a multisystem disorder affecting the heart, skin, joints and CNS.

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2
Q

Rheumatic Heart Disease (RHD?

A

RHD is a long-term complication of ARF.

 Major effect on health is due to damage to heart valves
(Commonly affected valve is the Mitral Valve).

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3
Q

Pathogensis of RHD?

A

The key risk factor is infection with group A streptococci (pyrogens)

Antibodies produced against the streptococcal antigens cause inflammation
in the endocardium, myocardium and pericardium, as well as the joints and
skin.

During an infection, monoclonal antibodies are formed against GAS antigens
mainly M-protein and N-acetyl glucosamine.
 Molecular Mimicry between antigens and human host tissue, these
antibodies can then cross-react with cardiac proteins as well as proteins in
synovial, neuronal, subcutaneous and dermal tissues.
 So, the condition is not due to direct infection of the heart or the
production of a toxin.

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4
Q

Clinical features of RHD?

A

The disease presents 2–4 weeks after the
initial GAS infection with fever, joint pain
and malaise.
 The diagnosis for acute rheumatic fever is
aided using the revised Jones Criteria:
 Two major criteria or one major and
two minor, plus  Evidence of a preceding streptococcal
infection:
 +ve throat culture.
 +ve rapid streptococcal
antigen/rising streptococcal
antibody titre (anti-streptolysin O).

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5
Q

Ddx for RHD?

A

The DDX is wide due to the multisystemic nature of the condition:
1. Infective endocarditis:
 The most important differential for the carditis of acute rheumatic fever.
 Systemically unwell with positive blood cultures .
2. Septic arthritis must be excluded in any arthropathy:
 Joints typically warm and tender with systemic upset usually a monoarthropathy
 Suspected infected joints should be aspirated for culture. 3. Juvenile idiopathic arthritis:
 Typically longer history than acute rheumatic fever with no preceding pharyngitis.
 Other systemic features such as conjunctivitis may be present.
 Positive autoimmune work up .
4. Chorea:
 Encephalitis: unusual behavior, pyrexia and convulsions.
 Drug-induced: dopamine antagonists in young women (e.g. metoclopramide).
 Wilson’s disease: liver disease and neuropsychiatric symptoms are prominent.

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6
Q

Needed investigations of RHD?

A

First-line:
To establish presence of streptococcal infection and carditis as well as to exclude infective endocarditis:
 Throat swab culture – often negative.
 Anti-streptococcal serology – antistreptolysin O (ASO) (most specific test).
 ECG – AV block, features of pericarditis.
 Blood tests – raised WBCs and acute phase reactants ( ESR/ CRP).
 Blood cultures: to exclude infective endocarditis.
 Chest X-ray: cardiomegaly; pulmonary congestion.
 Echocardiography as recommended by AHA and ESC .

 Second-line: To exclude other differential diagnoses:
 Systemic auto-antibodies in systemic lupus erythematosus (SLE).
 Copper and caeruloplasmin for Wilson’s disease.

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7
Q

Management of RHD( ARF)?

A

The WHO advocates the following five principles approach :
1-Antibiotics:
 A single dose of benzathine benzylpenicillin (1.2 million U IM) or
oral phenoxymethylpenicillin (250
mg 4 times daily for 10 days) should be given on diagnosis to eliminate any residual streptococcal
infection.
 If the patient is penicillin-allergic, erythromycin can be used.

2- Anti-inflammatory:
 NSAID a or Aspirin (ASA) is the first line: this usually relieves the symptoms of arthritis rapidly and a
response within 24 hours helps confirm the diagnosis.  Corticosteroids if no response to ASA, pericarditis or heart failure.  No evidence that corticosteroids are any better than aspirin.
 Management of Heart Failure and Valvopathy.

3-

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8
Q

When do we give antibiotic prophylaxis?

A

Long-term secondary prophylaxis is required to prevent chronic recurrence of acute rheumatic
fever and the onset of rheumatic heart disease.
 IM benzylpenicillin every four weeks is the most effective strategy
 Oral penicillin daily is an alternative , but non-adherence is an issue
 Duration of therapy (based on AHA guidelines):

 No carditis or valvular disease : five years, or until 21 years of age (whichever is longer)
 With carditis but no persistent valvular disease : ten years, or until 21 years of age
(whichever is longer)
 With carditis and persistent valvular disease : ten years, or until 40 years of age, although
lifelong prophylaxis may be needed.

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9
Q

What to give In patients with a history of ARF who have developed:
 Severe, symptomatic valvular disease,
 New York Heart Association class III or IV heart failure, or
 Ventricular dysfunction (ejection fraction <50 %). ?

A

AHA recommend prophylaxis with an oral antibiotic rather than IM penicillin G benzathine .

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10
Q

The arthritis of rheumatic fever typically respond to aspirin, if not respond to asa consider another diagnosis.

A
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11
Q

What is IE?

A

IE is an endovascular infection of cardiovascular structures , including
cardiac valves, atrial and ventricular endocardium, large intrathoracic vessels
and intracardiac foreign bodies, such as prosthetic valves, pacemaker leads.

More than 50% of patients are over 60 years of age .

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12
Q

If IE left untreated?

A

Without treatment, mortality approaches 100%.

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13
Q

How IE occur?

A

Endocarditis is usually the consequence of two factors:
1- the presence of
organisms in the bloodstream ( Bacteremia), and
2- abnormal cardiac
endothelium that facilitates their adherence and growth.

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14
Q

Pathogensis of IE?

A

Endothelial damage: Turbulent blood flow produced by certain types of
congenital or acquired heart disease, such as flow from a high- to a low-
pressure chamber or across a narrowed orifice, traumatizes the
endothelium.

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15
Q

What micrbiology that causes IE?

A

The three most common causes of IE
worldwide are staphylococci,
streptococci, and enterococci.

1- Staphylococcus aureus is the most
common cause of IE especially in
health care-associated IE and early
Prosthetic Valve Endocarditis.

.  2- Streptococcus Viridans is a common
cause of community-acquired IE and
Native Valve Endocarditis.

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16
Q

Which organsism causes IE especially in
health care-associated IE and early
Prosthetic Valve Endocarditis. ?

A

S. Auteus

17
Q

Which organism causes common
cause of community-acquired IE and
Native Valve Endocarditis.

A

Streptococcus Viridans

18
Q

Which organisms causes commonly IE in elderly?

A

Strp.bovis

19
Q

Which organism is always associated with large bowel malignancy in IE?

A

Streptococcus gallolyticus (previously known as Streptococcus
bovis)

20
Q

Risk factors of IE?

A

 Risk of Bacteremia:
 IV drug abuse, Indwelling venous catheter, Poor oral
hygiene, Hemodialysis and Prosthetic material in the heart (pacemaker, ICD).

 Abnormal Structure:
 Prior infective endocarditis, Rheumatic heart disease,
Bicuspid aortic valve, Valve replacement and congenital heart
disease.

21
Q

Cinical features of IE?

A

 Pyrexia is the most common symptom.

 Constitutional symptoms : malaise,
fatigue, anorexia, weight loss.
 Embolic phenomena: most often as a
result of subacute endocarditis.
 Pulmonary: pulmonary embolism,
lung abscess.
 Renal/spleen: infarction
.  CNS: stroke, meningitis.
 Bone: osteomyelitis.

22
Q

What is the most common symptom of IE?

A

Pyrexia

23
Q

What do we find in physical exam in IE patients?

A

 Extremities: Splinter hemorrhage,
Janeway lesion, Osler nodes, Petechiae.
 HEENT: Neurological assessment, Roth
spot, Conjunctival hemorrhage, Palate
petechiae.
 Neck: JVP.
 Precordium: Looking for new Murmur
(Regurgitation).
 Abdomen: Tender splenomegaly.
 Back: Vertebral tenderness.
 Device Examination.

24
Q

Always remember FEVER and NEW OR WORSENING MURMUR is IE until proven otherwise

A
25
Q

Needed invistgation for IE?

A

 First-line: To establish presence of bacteremia and evidence of
endocardial involvement:
 Blood tests: raised WCC, ESR, CRP and normocytic anemia.
 Urine dipstick: microscopic hematuria.
 CXR: Evidence of pulmonary edema or right sided IE related complications.
 ECG: 10% develop conduction problems; heart block may be a sign of an
aortic root abscess.
 Blood cultures.
 ECHO (TTE vs TEE).

 Second-line: To identify other potential etiologies:
 CT/MRI: CNS

 Nuclear imaging: positron emission tomography

Serology: if blood cultures are negative, Coxiella, Bartonella and
Brucella should be tested for.