ACUTE JOINT RHEUMATISM

ACUTE JOINT RHEUMATISM

ACUTE JOINT RHEUMATISM

Plan : 

            I. Definition

           II. Epidemiology

          III. Etiopathogenesis

          IV. Positive diagnosis

           V. Diagnosis 

          VI. Diagnostic criteria

         VII. Differential diagnosis

        VIII. Prognosis

           IX. Treatment

Goals :

1- Define acute rheumatic fever  

2- Describe the clinical signs of acute rheumatic fever polyarthritis. 

3. List and describe the manifestations of RAA. 

4. Know the methods of treating an ARF crisis 

5. Indicate the principles of RAA prophylaxis and specify their methods of application.

  1. Definition :
  • It is the set of inflammatory manifestations mainly affecting the heart, joints, CNS, linked to a delayed complication of a pharyngeal infection by group A beta hemolytic streptococcus (HBSA).
  1. Epidemiology :
    1. Frequency :
  • In industrialized countries, rheumatoid arthritis, which was very common at the beginning of the 20th century , has experienced a significant decline with the improvement of socio-economic conditions and the advent of antibiotics. Its incidence is currently very low.
  • In developing countries, RAA is endemic and constitutes a public health problem.
  • In Algeria (1990): Incidence of RAA = 3%
  1. Age :
  • It is a school-age disease that is observed between 5-15 years old.
  • It is rare before 4 years and after 30 years.
  1. Etiopathogenesis:
  • RAA is preceded (2-3 weeks before the outbreak) by a pharyngeal infection with SBHA.
  • Reinfection with SBHA in a patient who has already had an ARF flare reactivates the disease.
  • There is cross-antigenicity between myocardium and streptococcus.
  • Indeed, there is a structural analogy between proteins of the streptococcus capsule (protein M, polysaccharide C) and certain constituents of the myocardium (tropomyosin), joint antigens, and certain nerve cells of the caudate nucleus.
  • Role of family and genetic factors with predominance of certain HLA groups.
  1. Positive diagnosis:
    1. Extracardiac signs:
      1. General signs:

They are constant.

  • Moderate fever not exceeding 39°C.
  • Alteration of general condition
  • Asthenia, anorexia, moderate weight loss
  • Pallor.
  • Fever associated with endocardial involvement poses diagnostic problems with infective endocarditis.
  1. Skin signs:

Are rare

  • Meynet nodules:
    • Firm, rounded, painless nodules that are mobile relative to the subcutaneous plane.
    • They sit on the extension face of the large joints.
    • They disappear in less than a month.
    • They are most often associated with carditis.
    • They are not pathognomonic of RAA as they can be seen in SLE and RA.
  • Besnier’s erythema marginatum:
    • Pinkish, non-itchy, non-hardened macules, located on the trunk and at the roots of the limbs.
    • It is also most often associated with carditis.
  1. Joint signs:
    1. Arthritis:
  • In its typical form, it is an acute polyarthritis with significant local inflammatory signs, fleeting (each arthritis lasting only 3 days to 1 week), and migratory.
  • The joints usually affected are the medium-sized superficial joints such as the knees, ankles, wrists, but in fact all joints can be affected, from the small joints of the fingers and feet to deeper joints such as the hip, or even spinal arthritis at the lumbar or cervical level.
  • It evolves without sequelae or suppuration. 
  1. Arthralgia:
  • They are not accompanied by visible local inflammatory signs, but the spontaneous pain caused by joint movements most often leads to functional impotence. 
  • They are also mobile and fleeting, affecting the large joints.
  1. Sydenham’s chorea:
  • She is rare to touch girls willingly.
  • It can be seen during joint manifestations or isolation.
  • Its appearance is delayed compared to the outbreak (2 to 6 months after pharyngitis). The inflammatory signs have disappeared and the ASLO have returned to normal. It is therefore sufficient for the diagnosis of RAA.
  • It begins with mood swings and clumsiness.
  • Then to the state phase:
    • Ataxia, hypotonia.
    • Abnormal movements: Rapid, large involuntary movements located at the roots of the limbs. They are exaggerated during clinical examination and emotions, and diminish during sleep.
  • It disappears without after-effects in a few months.
  1. Biological signs:
    1. Inflammatory signs:
  • They are not very specific.
  • They demonstrate the progression of the disease, allowing treatment monitoring.
  • It seems that the appearance of carditis is to be feared especially when there are significant inflammatory signs with an ESR >60 mm in the 1st hour .
  • ESR may be falsely low in heart failure and falsely high in anemia.
  • Increased CRP, fibrinemia (> 5g/l), haptoglobin and α2-globulin.
  • Moderate inflammatory anemia: This is a good reflection of the duration of the development of the rheumatic disease.
  • Hyperleukocytosis with polymorphonuclear neutrophils.
  1. Signs of strep infection:
    1. Throat swab:
  • The search for SBHA in the throat swab is often negative because the RAA occurs 2-3 weeks after the pharyngeal streptococcal infection.
  • Rapid diagnostic test:
    • It is an immunological technique allowing the determination of specific SBHA antigens in throat swabs.
    • They are specific but less sensitive, requiring the sample to be cultured when the test is negative.
  1. Antistreptococcal antibodies:
  • An ASLO level > 250 IU/ml indicates a recent streptococcal infection.
  • The increase in the ASLO rate during 2 successive examinations spaced 15 days apart is more significant.
  • An ASLO level does not rule out the diagnosis, hence the importance of measuring other antistreptococcal antibodies such as antistreptodornase antibodies (ASDOR) and antistreptokinase antibodies.
  • Using all 3 tests increases sensitivity to 95%.
  1. Cardiac signs:
  • Carditis represents the major risk of the disease.
  • MI and aortic regurgitation occur contemporaneously with the ARF crisis, whereas MR and aortic stenosis occur after several years.
  1. Endocarditis:
    1. IM:
  • This is the most common condition.
  • Moderate or significant IM (Physiopathology, Diagnosis, evolution, treatment cf. IM).
  1. RM:
  • It occurs after several years, in adulthood, however in countries where rheumatic disease is endemic, childhood forms are not rare.
  • Cf. RM
  1. Aortic insufficiency:
  • It is most often associated with mitral valve disease.
  • Cf. IAo 
  1. Aortic stenosis:
  • It also occurs after several years.
  • It is often associated with aortic insufficiency 
  • Cf. RAo 
  1. Tricuspid injury:
  • Organic IT is exceptionally isolated. It is always associated with RT and often associated with mitral or aortic involvement.
  1. Polyvalvulopathies:
  • They are not rare, especially in countries where rheumatic disease is endemic.
  1. Rheumatic myocarditis:
  • It most often accompanies valvulopathy.
  • Muffled heart sounds, S3, congestive heart failure, cardiomegaly on telethorax.
  • Echocardiography: Global hypokinesia of the LV.
  • She improves rapidly with corticosteroid treatment.
  • The concept of rheumatic myocarditis is questioned by some authors and these pictures of heart failure would be linked to severe MI.
  1. Rheumatic pericarditis:
  • Pericardial friction
  • Repolarization disorders on the ECG
  • Dry pericarditis or pericardial effusion
  • It does not progress to constriction.
  1. Conductive disorders:
  • They are the witness of the inflammatory syndrome and myocardial damage.
  • usually nodal block and is generally limited to a simple lengthening of PR but can reach the second or third degree.
  • They regress rapidly under corticosteroid treatment.
  1. Rheumatic pancarditis:
  • It is an attack on the 3 layers of the heart.
  • It is rare.
  1. Diagnostic criteria:
    1. Jones criteria:
  • The Jones criteria should only be used for initial impairment.
  • RAA is very likely in the event of an association of 2 major criteria or one major criterion and two minor criteria necessarily associated with proof of a recent streptococcal infection.
  1. Major criteria:
  • Polyarthritis
  • Carditis
  • Erythema marginatum
  • Meynet’s nodule
  • Chorea
  1. Minor criteria
  • Arthralgia
  • Fever
  • Elevated ESR or CRP.
  • Lengthening of the PR.
  1. Recent streptococcal infection:
  • Significant elevation of antistreptococcal antibodies
  • Positive culture or rapid diagnostic test.
  • Recent scarlet fever.

ACUTE JOINT RHEUMATISM

  1. Differential diagnosis:
    1. In the face of polyarthritis:
  • Still’s disease (juvenile chronic arthritis): 
    • It may be accompanied by pericarditis but not endocarditis.
    • Fixed arthritis.
  • Others: LED, SPA, Lyme disease, PR, Malignant hematological diseases , sickle cell disease , Tuberculosis
  1. In front of a carditis:
  • Infective endocarditis: Echocardiography shows vegetations and blood cultures isolate the germ.
  • Valvular dystrophy .
  1. Evolution/prognosis:
    1. Prognosis of rheumatic flare-up:
  • The prognosis depends on whether or not carditis is present.
  • Relapses in the absence of prophylaxis are frequent, especially during the first 5 years, with the risk of the appearance or worsening of cardiac damage.
  • The prognosis is more serious if the relapse occurs in an already damaged heart.

ACUTE JOINT RHEUMATISM

  1. Prognosis of carditis:
  • Carditis may regress. But this is rare when heart failure and cardiomegaly appear during the acute phase.
  • Valvular lesions can progress even in the absence of relapse (hemodynamic disturbances, slow healing).
  • Classification of carditis:
    • Mild carditis: Mild mitral or aortic murmur, normal heart volume.
    • Moderate carditis: Intense murmur persisting after the acute attack. Mild cardiomegaly (RCT ≤ 0.55)
    • Severe carditis: Aortic insufficiency or significant MI. Significant cardiomegaly (RCT > 0.55).
  • The prognosis for rheumatic heart disease depends on the type and number of valves affected. 
  • Prognosis of IM, RM, IAo, RAo. See question.
  1. Treatment :
    1. Treatment of the thrust:
      1. General measures:
  • Rest is essential
  • Education of the patient and his family.
  • If heart failure: Symptomatic treatment with digital diuretic and vasodilator
  • If chorea: Neuroleptic, Haloperidol 0.2-0.5 mg/kg/day.
  1. Antibiotic treatment:
  • It ensures the removal of SBHA from the pharynx.
  • Benzathine-benzyl-penicillin (BBP): A single IM injection 600,000 IU if weight <30 kg 1,200,000 IU if weight ≥ 30 kg
  • Peni G IM for 10 days is an alternative to this treatment.
  • Oral route if injections are contraindicated (anticoagulant treatment) or if the child is pusillanimous: Peni V 50000-100000 IU/Kg/day in children and 2000000 IU/day in adults, divided into 3 doses at mealtimes, for 10 days.
  • If allergic to penicillin: Erythromycin 30 mg/kg/day divided into 3 doses at mealtimes, for 10 days.

ACUTE JOINT RHEUMATISM

  1. Anti-inflammatory treatment:
  • Prednisone 2mg/kg/day without exceeding 80 mg/day divided into 3 doses at mealtimes.
  • Adjuvant treatment: Low sodium, high protein diet. Potassium and calcium supplementation. Gastric dressing.
  • Duration of treatment:
    • In the absence of carditis:
      • Attack treatment: 2 weeks. The ESR normally returns to normal after this period.
      • Maintenance treatment: Gradual reduction of doses (5mg/week) over 6 weeks.
    • If carditis: 3-week attack treatment
      • If moderate carditis: 6-week maintenance treatment.
      • If severe carditis: 9-week maintenance treatment
  • Aspirin (3g/day) is proposed by some authors in forms without cardiac involvement or as a follow-up to corticosteroids to avoid a rebound.
  1. Prophylaxis:
    1. Primary prevention:
  • Treatment of strep throat:
    • Systematic antibiotic treatment with a BBP injection (see above)
    • In the United States, rapid diagnostic tests make it easier to detect strep throat.
  • Improvement of socio-economic conditions.
  1. Secondary prevention: Relapse prevention
  • BBP IM every 21 days.
  • Peni V 500,000 IU 2f/day orally
  • Erythromycin 250 mg/day twice a day orally.
  1. National plan to combat RAA:
  • It was established in 1990.
  • Its aim is to reduce the incidence of rheumatic fever and rheumatic heart disease through better organisation of health structures.

ACUTE JOINT RHEUMATISM

Deep cavities may require root canal treatment.
Interdental brushes effectively clean between teeth.
Misaligned teeth can cause chewing problems.
Untreated dental infections can spread to other parts of the body.
Whitening trays are used for gradual results.
Cracked teeth can be repaired with composite resins.
Proper hydration helps maintain a healthy mouth.
 

ACUTE JOINT RHEUMATISM

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