Rheumatic_Heart_Disease by Ananya Singha

Rheumatic heart disease, its type and its management

1. Ananya Singha B.P.T Final Year

2. OBJECTIVES Introduction Epidemiology Pathophysiology Classification Pericarditis Myocarditis Endocarditis (valvular) Endocarditis (mural) Clinical features Physical examination Investigation Modified jones criteria Management

3. INTRODUCTION Rheumatic heart disease: It is heart damage due to rheumatic fever. The chronic stage of rheumatic fever involves all the layers of the heart (pan carditis) causing major cardiac sequelae. Rheumatic fever : It is a systemic, post-streptococcal, non suppurative, inflammatory disease mainly affecting the heart, joints, central nervous system, skin & subcutaneous tissues. It is an acute, immunologically mediated, multisystem, inflammatory disease that occurs a few weeks following an episode of group A streptococcal pharyngitis.

4. EPIDEMIOLOGY Rheumatic fever mostly affects children and adolescents in low- and middle-income countries, especially where poverty is widespread and access to health services is limited. People who live in overcrowded and poor conditions are at greatest risk of developing the disease. Where rheumatic fever and rheumatic heart disease are endemic, rheumatic heart disease is the principal heart disease seen in pregnant women, causing significant maternal and perinatal morbidity and mortality. Pregnant women with rheumatic heart disease are at risk of adverse outcomes, including heart arrythmias and heart failure due to increased blood volume putting more pressure on the heart valves. It is not uncommon for women to be unaware that they have rheumatic heart disease until pregnancy. Despite it being eradicated in many parts of the world, the disease remains prevalent in sub-Saharan Africa, the Middle East, Central and South Asia, the South Pacific, and among immigrants and older adults in high-income countries, especially in indigenous peoples.

5. PATHOPHYSIOLOGY Infection with Streptococcus pyogenes, a beta-hemolytic bacterium that belongs to  Lancefield serogroup A

6. CLASSIFICATION * If all layers of heart is affected then it is called PAN CARDITIS.

7. RHEUMATIC PERICARDITIS Pericardium gets inflamed(both visceral & parietal) → capillaries develops high permeability → leakage of large protein molecules like fibrinogen → fibrinogen polymerises → fibrin string formation (thread like structure) → fibrinous pericarditis. When fever reduces the fibrin is cut down by plasmin and the patient gets well. There is no long term complication. ‘BREAD AND BUTTER APPEARANCE’

8. RHEUMATIC MYOCARDITIS Aschoff bodies are present in the myocardium(pathognomonic of RHD). They are small pinhead immune-mediated granulomas. Usually present in perivascular connective tissues. On the histopathology slide, there’s swollen collagenous fibers around inflammatory cells, there are special types of macrophages that contain ribbon-like chromatin ( looks like caterpillars), which are called Anitchkov cells. Myocarditis develops during acute fever (most dangerous). Myocardium becomes inflamed it becomes loose & flabby, hence can not pump properly which leads to congestive cardiac failure eventually.

9. RHEUMATIC VALVULAR ENDOCARDITIS Vegetations (nodules) are present in heart valves which are sterile in nature. Valves also show thickening and loss of translucency. Vegetations are also seen in infective endocarditis, nonbacterial thrombotic endocarditis & and Libman -Sacks endocarditis but in RHD they are the smallest (<3mm). Mitral valves are most commonly involved ( ‘fish mouth’ appearance). ‘FISH MOUTH’ APPEARANCE ON MITRAL VALVE

10. RHEUMATIC MURAL ENDOCARDITIS MacCallum’s patch is seen ( wrinkled patch). It is seen in the endocardial surface in the posterior wall of the left atrium just above the posterior leaflet of the mitral valve. These plaques appear as  map-like areas of thickened, roughened, and wrinkled part of the endocardium in the left atrium . Perhaps they are caused by regurgitant jets of blood flow, due to incompetence of the mitral valve.

11. CLINICAL FEATURES

12. PHYSICAL EXAMINATIONS Severity and assessment of heart failure (tachypnoea, tachycardia, increased JVP, oedema, hepatomegaly) Presence of atrial fibrillation must be assessed. Auscultation of heart sound to rule out any valvular deformity.

13. INVESTIGATIONS HISTORY TAKING : history of sore throat. PHYSICAL EXAMINATIONS : ECG to assess the abnormal cardiac rhythm Chest x-ray to assess the size of the heart chambers and detect pulmonary congestion. Echocardiography (gold standard) to confirm the diagnosis and detect any valve damage and its severity. Additional lab tests include CBC, liver function test, renal function test, electrolytes ( na and k) etc

14. MODIFIED JONES CRITERIA MAJOR CRITERIA Carditis Subclinical Echo with Doppler must be done in all cases of confirmed and suspected acute rheumatic fever as auscultatory findings take time to develop. Subclinical carditis seen on echo is now considered major diagnostic criteria. Clinical Pericarditis(m/c) 5-15 yrs , recurrent sore throat. Chest pain at rest, pericardial friction rub. ST elevation on ECG, concave upward is present in all leads except aVR . 2. Arthritis . 3. Syndenham's chorea 4. Subcutaneous nodules 5. Erythema marginatum

15. MINOR CRITERIA Fever (>38.5c) Arthralgia Increased ESR + ve CRP Prolonged PR interval (1 st degree heart block) ESSENTIAL CRITERIA ASO titer >200 IU/ML

16. MANAGEMENT

17. Other symptoms management-