Pericardial diseases

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Pericardial diseases

  1. 1. 1) Anatomy of pericardium 2) Overview of pericardial disease 3) Clinical presentation 4) Acute pericarditis 5) Chronic pericarditis
  2. 2.  Normal amount of pericardial fluid: 15-50 cc  Two layers:  Outer layer is the parietal pericardium and consists of layers of fibrous and serous tissue  Inner layer is visceral pericardium and consists of serous tissue only
  3. 3.  Fibroelastic sac consisting of 2 layers  Visceral at epicardial side  Parietal at mediastinal side  Pericardial fluid formed from ultrafiltrate of plasma
  4. 4.  Acute Pericarditis  Chronis pericarditis  Pericardial Effusion
  5. 5. 1)Infection 2)Radiation 3)Neoplasm 4)Myocardial intrinisic disease 5)Trauma 6)Autoimmune 7)Drugs 8)Metabolic *viral, autoreactive/autoimmune, and neoplastic most common diagnosis
  6. 6. Viral -adenovirus -enterovirus -cytomegalovirus -influenza -hepatitis B -herpes simplex -echovirus -mumps Mycoplasma Fungal Parasitic Bacterial -staphylococcus -streptococcus -pneumococcus -haemophilus -neisseria -chlamydia -legionella -tuberculous -lyme disease
  7. 7. Radiation Neoplasm -metastatic -primary cardiac -paraneoplastic Cardiac -early infarction -Dressler’s -myocarditis -aortic dissection Trauma -blunt -iatrogenic (perforations, post- surg) Autoimmune -rheumatic disease -non-rheumatic -Wegners, sarcoid, IBD
  8. 8. Drugs -drug induced lupus hydralazine isoniazid procainamide -doxorubicin -phenytoin Metabolic -hypothyroid -uremia -ovarian hyperstimulation
  9. 9.  Serous  Fibrinous  Purelent  Hemorrahgic  Caseous
  10. 10.  50-200ml exudate  Etiology unknown
  11. 11.  Scant acute and ch inflammatory infiltrate  Fluid reabsorb leaving any residual change
  12. 12.  Most commonly seen in MI  Associated with friction rub
  13. 13.  Fibrin strands  Inflammatory exudate  Congested capillaries  Exudate can completely resolve or can organize leaving delicate, stringy adhesions or plaque like thickening.
  14. 14.  Usually signifies bacterial, fungal or parasitic infection  Direct extension, hematogenous or lymphatic spread.  Common organisms streptococci, staphylococci and pneumococci
  15. 15.  400- 500 ml  Thin to creamy pus  Erythematous, granular surface  Can produce constrictive pericarditis
  16. 16.  Exudate of blood admixed with fibrinous to supparative effusion  Most commonly it follows cardiac surgery or associated with tuberculosis or malignancy  It organize with or without calcification
  17. 17.  Due to tuberculosis  Typically by direct extension from neighboring lymph nodes or less commonly mycotic infection  Lead to fibro calcific constrictive pericarditis.
  18. 18.  Central caseous necrosis  Epitheliod histiocytes forming granulomas  Giant cells.
  19. 19.  Healing of acute lesions  Adhesive medistinopericarditis  Constrictive pericarditis
  20. 20.  Clinically significant  Pericardial sac obliterated  Parietal layer is tethered to medistinal tissue  Heart so contract against the surrounding attached structures with hypertrophy and dilatation.
  21. 21.  Clinically significant  Thick dense fibrous obliteration with calcification of the pericardial sac encasing the heart limiting diastolic expansion and restricting cardiac output.
  22. 22.  Normal in patients with acute pericarditis unless pericardial effusion is present  Requires 200cc of fluid
  23. 23.  the historic yield of diagnostic evaluation is low, typically only in 16% of patients is etiology determined.  evaluation of pericardial fluid and tissue with tumor markers, PCR, immunohistochemistry, flourescence-activated cell sorting has shown a trend toward higher yield of diagnosis
  24. 24. 1) Chest pain  Sudden onset  localized to anterior chest wall  pleuritic  sharp  Positional: may improve if pt leans forward, worse with lying flat 2) Cardiac auscultation: Pericardial friction rub  Present in up to 85% of pts with pericarditis without effusion  friction of the two inflamed layers of pericardium, typically triphasic rub, heard with diaphragm of stethoscope at left sternal border 3) Characteristic ECG changes 4) Pericardial effusion
  25. 25.  Elevated C reactive protein level  strong correlation - normal CRP makes acute pericarditis diagnosis less likely  Elevated CK, CK-MB, and Troponin  Often elevated Troponin alone  Indicates inflammation of myocardium just beneath the visceral pericardium  Not associated with worse outcomes  Leukocytosis
  26. 26.  51yo man with acute onset sharp substernal chest pain two days prior
  27. 27.  Low voltage and Electric Alternans
  28. 28.  Pressure in pericardium exceeds pressure in the cardiac chambers, lower chamber atria affected before higher pressure ventricles  Compressive effect is seen best in the phase when the intrachamber pressure is lowest – systole for atria and diastole for ventricles  Diagnostic techniques  2D looking for RA/RV collapse during diastole  M-mode for RA/RV collapse during diastole  Doppler of Mitral and Tricuspid inflow  Mitral inflow to decrease by 25% with inspiration  Tricuspid inflow increased by 40% with inspiration  IVC diameter fails to increase with inspiration
  29. 29.  www.bidmc.org  www.heartydog.co.uk  www.budjzdorov.org.ua  www.histopathology-india.net

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