Rheumatic Fever PDF

Rheumatic fever Definitions: Rheumatic fever (RF) is an acute immune-mediated, multisystem, inflammatory disease that may follow a group A– hemolytic streptococcal infection of the pharynx when it is no adequately treated ○ Joints, skin the central nervous system, and heart a...

Rheumatic fever Definitions: Rheumatic fever (RF) is an acute immune-mediated, multisystem, inflammatory disease that may follow a group A– hemolytic streptococcal infection of the pharynx when it is no adequately treated ○ Joints, skin the central nervous system, and heart are targets for inflammation ○ The most serious aspect of RF is inflammation of the valves of the heart (i.e., valvulitis) that can progress to valvular deformities and cardiac dysfunction, a potential complication of RF known as rheumatic heart disease. ○ RF is rare before the age of 4 and after age 40. ○ RF and RHD continue to be major health problems in many underdeveloped countried of the world where poverty, inadequate healthcare, poor nutrition and crowded living conditions exist ○ It has been estimated that the worldwide population of people currently living with RHD is 15–20 million. ○ There is no gender predilection for RF. ○ Native Hawaiians and Maoris (both of Polynesian descent) have a higher incidence of RF than do other racial/ethnic groups. ○ Otherwise, race (when controlled for socioeconomic variables) has not been reported to influence the incidence of the disease. ○ The prevalence of RHD in the United States is now 5 cases per 100,000 individuals. Causes and risk factors: ○ There is only one cause of RF—exposure to group A β-hemolytic streptococci—which initially leads to a sore throat (i.e., pharyngitis). ○ Streptococcal infections of the skin do not cause RF. ○ Poverty, crowded living conditions, and poor personal hygiene are major environmental risk factors. ○ RF tends to run in families, lending support to the concept of genetic predisposition. Pathophysiology ○ RF may, in fact, be an autoimmune disorder ○ The bacteria responsible for strep throat causes the host to develop antibodies against its own tissue ,infiltrating the cardiac cells, leading to cardiac complication, common to all of these tissues is a microscopic lesion known as an Aschoff body, a localized area of cell death surrounded by cells of the immune system. ○ Inflammatory lesions of the joint ○ However, involvement of the valves of the heart produces permanent and often disabling complications. ○ The mitral valve alone is affected in up to 60% of cases, and combined lesions of the aortic and mitral valves occur in 20% of patients. ○ Tricuspid involvement occurs with mitral or aortic disease in approximately 10% of cases. ○ The pulmonary valve is rarely affected. ○ During the acute phase of RF, valves become red and swollen. ○ Shortly thereafter, scar tissue is produced that tends to contract and cause rigidity and deformity of valve leaflets.  ○ In some cases, the edges of the valve leaflets (i.e., commissures) fuse, causing valvular dysfunction Diagnosis: Clinical Manifestations and Laboratory Tests: ○ Clinical manifestations of pharyngitis appear 1–5 days following exposure to the infectious agent and include a sore throat, difficulty in swallowing (i.e., dysphagia), and a high-grade fever (i.e., 101°F). ○ Physical examination often reveals a red pharynx, swollen tonsils with tonsillar exudates (i.e., pus) and vesicles (i.e., blister-like lesions), cervical lymphadenopathy, and a widespread scarlet rash (i.e., scarlet fever). ○ Throat cultures taken from the surface of the tonsils and posterior wall of the pharynx are usually positive for group A streptococcus. ○ However, standard tests sometimes require up to 48 hours before results are available. ○ Serum antistreptolysin O titer (ASO) Is the most sensitive test for the diagnosis of Group A strep. ○ Newer tests that detect group A streptococcal antigens (i.e., latex agglutination or enzyme immunoassay) can be completed in less than 1 hour and are highly specific (90%) but are limited in their sensitivities (i.e., the person may be recently infected but test results are negative). ○ A negative antigen test should be confirmed with a throat culture when streptococcal pharyngitis is suspected. ○ No single laboratory test, sign, or symptom is diagnostic for RF; diagnosis is based on the Jones’ criteria, which were initially established in 1955 and most recently revised in 1992 by the American Heart Association. ○ The presence of at least two major clinical manifestations or one major and two minor criteria appearing 1–5 weeks after streptococcal infection of the pharynx establishes the diagnosis ○ Major manifestations consist of: ○ Carditis ○ erythema marginatum ○ subcutaneous nodules ○ Sydenham chorea arthritis. Minor signs include:  ○ Fever ○ Polyarthralgia ○ reversible prolongation of the PR interval with electrocardiogram (ECG), increased erythrocyte sedimentation rate (ESR) either evidence of an antecedent -hemolytic streptococcal infection or a history of RF. They may persist for weeks and are indistinguishable from the skin nodules characteristic of rheumatoid arthritis. ○ The least common (only 3% of cases) but clearly the most definitive sign of RF is: Sydenham chorea:—involuntary, spasmodic, irregular movements of primarily the tongue and upper extremities. ○ Occasionally, these movements are accompanied by slow, writhing, involuntary movements of the hands and feet. ○ Facial grimaces are common. ○ Children with chorea are often fidgety, cry easily, walk clumsily, and tend to ○ drop items. An elevated white blood cell count and C-reactive protein (CRP) concentration when cardiac and joint symptoms are prominent are also consistent with the inflammatory reaction of RF. ○ The first sign that the patient has developed valvular disease is a heart murmur. ○ A thorough physical examination is often all that is required to diagnose RHD, but echocardiography will reveal thickening of valve cusps, valvular stenosis, regurgitation, and the earliest stages of heart chamber dilation. Fewer than 5% of patients have symptoms that persist 6 months or longer. ○ Fever (minor) ○ Chorea (major) ○ Arthralgia (minor) ○ Polyarthritis (major) ○ Elevated sedimentation rate; ○ C-reactive protein, leukocytosis (minor) ○ Erythema marginatum (major) ○ Subcutaneous nodules (major) ○ Carditis (major) ○ History of previous rheumatic fever; prolonged P-R interval (minor) rate for an episode of RF approaches 2%, and death usually results from a carditis-induced arrhythmia. Prognosis is poor if the patient develops cardiomegaly, heart failure, and pericarditis. Appropriate therapy ○ Bed Rest for the patient is necessary until body temperature returns to normal without the aid of antipyretic drugs and the ESR, resting pulse rate, and ECG are normal. ○ Although they have no effect on the clinical course of the disease, salicylates (e.g., aspirin) dramatically reduce fever and reduce joint pain and swelling associated with RF. ○ Oral prednisone rapidly improves joint symptoms and is indicated when salicylates are ineffective, but corticosteroids do not preventinjury to the heart. ○ RHD results from a single severe attack of RF or repeated attacks that cause additive damage to valves.  ○ These patients should also receive prophylactic antibiotics preceding the cleaning of teeth, dental extractions, and various urologic and surgical procedures to prevent serious, potentially life-threatening heart infections (infective endocarditis) that develop on deformed cardiac valves. ○ With mitral valve disease, it is important to identify the onset of cardiac arrhythmias that promote blood clot (i.e., thrombus) formation in order to begin anticoagulation efforts. ○ In patients with symptomatic RHD, surgical repair of damaged valves may be necessary. ○ As a result, the prevention of recurrent episodes with antibiotics is critical. 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