RHEUMATIC FEVER & RHEUMATIC HEART DISEASE
I. INTRODUCTION
Rheumatic Heart disease is the main topic of our case study, wherein this study it will give information about Rheumatic Heart disease and what lies behind it, which includes its definition, etiology, pathophysiology, signs and symptoms, prevention and treatment of this particular disease. On the other hand our group decided to choose this case study regarding Rheumatic Heart Disease for us to be able to gain and impart knowledge to other people especially to our patients. We all know nowadays the widespread of heart diseases can lead to some serious complications which can even lead to death. That’s why it’s very important to be educated with regards to heart diseases and Rheumatic Heart disease is one of them. That’s why this case study is really essential for us it is because it will help us to prevent and treat any further complications of this particular disease.
II. DEFINTION OF DISEASE
Ø Is a diffuse inflammatory disease that follows a throat infection with Group A (ß hemolytic streptococcus).
Ø Most serious aspect of rheumatic fever is the development of chronic valvular disorders. In short RHEUMATIC HEART DISEASE is a sequeiae of rheumatic fever.
III. ETIOLOGY:
Ø Rheumatic fever is a disease of school age children. Incidence of acute rheumatic fever peaks between ages 5-15 years old. The disease usually follows an inciting streptococcus throat infection by 1-4 weeks.
Ø Rheumatic fever also follows a streptococcal infection of the nasopharynx.
Ø Rheumatic fever can present as an AUTE STAGE, RECURRENT PHASE & CHRONIC DISORDER.
ACUTE STAGE
Ø Includes history of streptococcal throat infection & subsequent involvement of mesenchymal connective tissue of the heart, blood vessels, joints & subcutaneous tissues.
Ø The presence of lesion called ASCHOFF BODY is a particular characteristic of the presence of rheumatic myocarditis. The aschoff body is a localized area of necrosis surrounded by immune cells. This phase resolves within 12 weeks.
RECURRENT PHASE
Ø Usually involves extension of the cardiac effects of the disease
CHRONIC PHASE
Ø Is characterized by permanent deformity of the heart valves & is a frequent cause of mitral valve stenosis.
IV. 5 Major Manifestations of Rheumatic Fever:
- CARDITIS
Ø It is the most destructive consequence of this disease. Characteristics include; a significant murmur, cardiomegaly, pericarditis that produces a friction rub & CHF. Chest pain due to pericardial inflammation may be present.
- POLYARTHRITIS
Ø Most common finding; characterized by migratory arthritis usually of the larger joints like the knees, ankles, elbows & wrist; responds dramatically (within 48 hrs.) to salicylates; in untreated cases, the arthritis last about 4 weeks.
3. CHOREA/ SYNDEHAM’S CHOREA/ ST. VITUS DANCE
Ø Is a major CNS manifestation characterized by spontaneous rapid, purposeless, jerking movements that interfere with voluntary activities. Facial grimaces are common & even speech maybe affected. The chorea is self-limiting, usually within a matter of weeks or months.
4. ERYTHEMA MARGINATUM
Ø Map like macular areas most commonly seen on the trunk or inner aspect of the upper arm & thigh. Skin lesions are present only in about 10% transitory & disappear during the course of the disease.
- SUBCUTANEOUS NODULES
Ø Nodules 1-4 cm. in size, hard painless, & freely moveable, usually over lie the extensor muscle of the wrist, elbow, ankle, & knee joints. Subcutaneous nodules are rare, but when present, they most often occur in people with CARDITIS.
V. Minor Manifestations of Rheumatic Fever:
- fever
- arthralgia
- elevated levels of acute phase reactants
- prolonged PR interval in ECG
- body malaise
- weight loss
- anorexia
VI. Clinical Manifestation:
Ø Signs & symptoms may include fever; migratory joint pain, skin lesions, firm movable, nontender subcutaneous nodules near tendons or bony prominences of joints; chorea (later symptom); or pleural friction rub and pain.
Ø The patient may also have a heart murmur. This may be a systolic murmur of mitral regurgitation (high-pitched, blowing, holosystolic, loudest at apex, possibly radiating to the anterior axillary line) alternatively, the patient may have a midsystolic murmur (caused by stiffening & swelling of the mitral leaflet) or occasionally a diastolic murmur of aortic regurgitation (low-pitched, rumbling, almost inaudible)
VII. Pathophysiology:
Ø Rheumatic fever produces a diffuse, proliferative & exudative inflammatory process. In rheumatic fever, there is involvement of the heart, joints, subcutaneous tissue, CNS & skin. Although the exact pathogenesis is not clear, it is probably through an abnormal humoral & cell-mediated response to streptococcal cell-membrane antigens. These antigens bind to receptors on the heart, tissues & joints, which begins the autoimmune response. The inflammatory process often produces permanent & severe heart damage.
Ø Rheumatic fever produces carditis or inflammation of the heart. This carditis affects the pericardium, epicardium, myocardium & endocardium. There may be surrounded Aschoff bodies, which are minuscule nodules with localized fibrin deposits surrounded by areas of necrosis in the myocardium that are due to the inflammation of the rheumatic fever. Endocardial inflammation causes swelling of the valve leaflets that leads to valve dysfunction & murmurs. Small bacterial vegetation form on the valve tissues, rough eroded areas of the valves attract platelets which adhere & form platelet fibrin clumps that eventually cause scarring & shortening. The valves lose their elasticity & cardiac function is impaired.
Ø First, the damaged valve may become narrowed or stenosed. This increases the cardiac workload because higher pressure must be generated to propel blood through the narrow valve.
Ø Second, the valve leaflets may become so short that they cannot close securely. As a result, blood regurgitates through the damaged valve into the chamber from which it was ejected. Both valvular stenosis & regurgitation eventually cause heart failure.
VIII. Diagnosis & Treatment:
Ø Diagnosis is based on Jones Criteria. This criteria was developed because no single laboratory test, sign or symptom is pathognomonic of the disease although several combinations of them are diagnostic.
Ø According to this criteria, a high probability of Rheumatic fever exist if there is presence of 2 major signs & symptoms or 1 major & 2 minor signs & symptoms accompanied by evidence of a preceding group A streptococcal infection.
Ø Evidence of a streptococcal infection is established through the use of throat culture positive for Group A streptococcus.
IX. Laboratory Findings:
1. Increase ASO Titer (Anti- Streptolysin O) indicative of Streptococcal infection
2. Increase ESR (Electrolyte Sedimentation Rate) – indicative of inflammation
3. Positive CRP (C-reactive protein)
X. DRUG STUDY
DRUG NAME | MODE OF ACTION | NURSING CONSIDERATION |
GN > Penicillin BN > Penadur Classifications: Antibiotic, Penicillin
| > A natural penicillin that inhibits cell-wall synthesis during microorganism multiplication. Bacteria resist penicillins by producing penicillinases-enzymes that convert penicillins to inactive penicillic acid. > exhibits antipyretic, anti-inflammatory, and analgesic effects. The antipyretic effect is due to an action on the hypothalamus, resulting in heat loss by vasodilation of peripheral blood vessels and promoting sweating. > Decreases inflammation, mainly by stabilizing leukocyte lysosomal membranes; suppresses immune response; stimulates bone marrow; and influences protein, fat, and carbohydrate metabolism. | > Use cautiously in patients with other drug allergies, especially to cephalosporins (possible cross-sensitivity), and in those with GI disturbances. Before giving drug, ask patient about allergic reactions to penicillins. However, a patient can have an allergic reaction even if he has never had one before. Obtain specimen for culture and sensitivity tests before giving first dose. Therapy may begin pending results. Give drug at least 1 hour before a bacteriostatic antibiotic. Periodically assess renal and hematopoietic function in patients receiving long-term therapy. Observe patient closely. With large doses and prolonged therapy, bacterial or fungal superinfection may occur, especially in geriatric, debilitated, or immunosuppressed patients. The American Heart Association considers amoxicillin the preferred agent for endocarditis prophylaxis because GI absorption is better and serum levels are sustained longer. Penicillin V is considered an alternative agent. Alert: Don't confuse drug with polycillin, penicillamine, or the various types of penicillin. > Instruct patient to take entire quantity of drug exactly as prescribed, even after he feels better. Tell patient to take drug with food if GI distress occurs. Advise patient to notify prescriber if rash, fever, or chills develop. A rash is the most common allergic reaction.
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