Peak incidence 5-15yrs Q
Occur due to pharyngeal infection with Lance field Group A Beta haemolytic streptococci Q triggers rheumatic fever 2-4wks Q later, carbohydrate cell wall of the streptococcus cross reacts with valve tissue (antigenic mimicry Q) and may cause permanent damage to the heart valves.
- Rheumatic fever is not a communicable disease.
- It is more common in Low socioeconomic people.
- Primary attack rate is 3%
- Secondary attack rate is 15 to 50%
Diagnosis revised Jones criteria.
- Hallmark is McCallum patch.
- Patient may have Aschoffâ€™s nodule which has Anitschkow myocyte.
Important points: (Pathology of rheumatic fever)
- Aschoff nodules
- MacCallum patch
- Fibrinous pericarditis
- Benzylpenicillin 0.6-1.2g IM stat then penicillin V 250mg/6h orally
- Analgesic for carditis/arthritis. Aspirin 100 mg/kg/d in divided doses. For 6wks. Toxicity causes tinnitus, hyperventilation, Metabolic acidosis
- Steroids Q. Are specially used if carditis is there with or without CHF.
- Valproate, carbamazepine for the chorea
Secondary prophylaxis Penicillin V 250mg/12h PO until no longer at risk (>30yr Alternative: sulfadiazine, erythromycin.
- Surgical replacement of mitral and/or aortic valve during acute rheumatic fever results in a rapid control of CCF and decrease in heart size, despite investigational evidence for ongoing active rheumatic fever. (AIIMS May 11)
- The surgical findings thus indicate that it is the acute hemodynamic overload secondary to valvar regurgitation, which is responsible for CCF and the morbidity and mortality of acute rheumatic.
Other important conditions associated with streptococcal infection.
- Post streptococcal reactive arthritis.
- PANDAS (Pediatrics autoimmune neuropsychiatry disorder associated with Streptococci)