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    Pericarditis Pericarditis Presentation Transcript

    • MYOCARDITISBYDr. Mahadev HaraniMBBS, M.Phil, FCPS.Professor Pathology,LUMHS Jamshoro.
    • Diverse group of pathologic entities in which microorganisms and/or an inflammatory process cause myocardial injury.
    • ETIOLOGY • Viral • Non-viral, Trypanosoma, Trichinosis, Toxoplasmosis, Diphtheria. • Non-Infectious due to Hypersensitivity reactions. • Drugs.Antibiotics, Diuretics and anti Hypertensive. Also associated with systemic diseases of immune origin. RF, SLE, polymyositis. Cardiac sarcoidosis and rejection of transplanted heart.
    • MORPHOLOGYAcute phase heart may be normal or dilated. Some hypertrophy may be present.In advance stages of disease ventricular myocardium is flabby and often mottled with minute hemorrhagic lesions.Mural thrombi in any chamber.During active disease myocarditis is mostly associated with interstitial inflammatory infiltrate associated with focal myocyte necrosis.
    • Continued Lymphocytic infiltrate is most common and Endomyocardial biopsy is diagnostic.Lymphocytic myocarditis is most common. If the patient survives the acute phase of myocarditis, the inflammatory lesions either resolve, leaving no residual changes, or heal by progressive fibrosis.Hypersensitivity myocarditis has interstitial infiltrate principally perivascular, composed of lymphocytes, macrophages and eosinophils.
    • Giant-cell myocarditis. characterized by widespread inflammatory cellular infiltrates containing multinucleate giant cells (formed by macrophage fusion) interspersed with lymphocytes, eosinophils, and plasma cells.Myocarditis of chagas disease show parasite trypanosomes accompanied by an inflammatory infiltrate of neutrophils, lymphocytes, macrophages, and occasional eosinophils
    • CLINICAL FEATURESAsymptomatic, recover completely.Symptomatic, heart failure, arrhythmias and sudden death.Symptoms of fatigue, dyspnea, palpitation, precordial discomfort and fever.c/f mimic acute MI.Occasionaly dilated cardiomyopathy is late complication.
    • Other causes of myocardial diseaseCytotoxic drugs.Catecholamines, Amyloidosis, Iron over load, Hyper and hypothyroidism.
    • PERICARDIAL DISEASEDiseases of the pericardium include inflammatory conditions and effusions.Isolated pericardial disease is unusual, and pericardial lesions are almost always associated with disease in other portions of the heart or surrounding structures, or are secondary to a systemic disorder.1)Fluidaccumulation 2)Inflammation 3)Fibrous constriction.Normally fluid 30-50ml thin, clear, strans colomned fluid.
    • Serous fluid :Pericardial effusionBlood :HemopericardiumPus :Purulent Pericarditis500ml, chronic globular enlargement.In acute state 200-300ml produce compression due to ruptured MI or aortic dissection
    • PERICARDITISInflammation of pericardium.Primary Rare, viral in origin.Secondary Due to cardiac diseases, thoracic, systemic, metastases, surgical procedures.
    • Causes.INFECTIVE:Virus, pyogenic bacteria, TB, Fungi, Parasites.IMMUNOLOGICALLY MEDICATED: RF, SLE, Scleroderma, Drug hypersensitivity reactionMISCELLANOUS:MI, uremia, Neoplasia, Trauma, Radiation
    • ACUTE PERICARDITISSerous Pericarditis: Produced by non- infectious inflammatory disease such as RF, SLE, Scleroderma, tumor, uraemia.Bacterial pleuritis may cause sufficient irritation of pericardium.Viral Infection antedates pericarditis.MORPHOLOGY: Inflammatory reaction with few neutrophils,lymphocytes and histiocytes.
    • Volume of fluid between 50-200 ml,accumulates slowly.Organization into fibrous rarelr occurs.
    • FIBRINOUS AND SEROFIBRINOUS PERICARDITISSerous Fluid mixed with fibrinous exudate.Common Causes: Acute MI, Dressler syndrome, Uraemia, Chest radiation, RF, SLE, Trauma.IN FIBRINOUS PERICARDITISThe surface is dry with fine granular roughening.
    • In sero-fibrinous carditisIntense inflammatory process, produces large amount of yellow to brown fluid with presence of leukocytes and red cells with fibrin.Clinically precardial friction rub heard.Pain, febrile reaction with signs of cardiac failure.
    • Purulent or suppurative PericarditisInvasion of pericardial space by microbes.a) Direct extension from empyemab) Seeding from bloodc) Lymphatic extensiond) Direct extension during cardiotomyImmunosupression pre-disposes to infection.
    • ContinuedExudate ranges from thin cloudy fluid to pus 400-500ml, in volume.Serosal surface red, granular and coated with exudate.Microscopically acute inflammatory reaction seen.Scarring produce constrictive pericarditis.Signs of systemic infection noticed.
    • Haemorrhagic PericarditisBlood mixed with fibrinous or suppurative effusion due to neoplasm. Cytological examination needed.Also seen in bacterial infection due to bleeding diathesis.Also due to cardiac surgery.
    • Caseous PericarditisRare,due to tuberculosis until proved other wise.It leads to chronic constrictive pericarditis
    • U Y O K ANTH