1. Infective Endocarditis
Faculty of Medicine
University of Brawijaya
Malang

2. INTRODUCTION
The term ‘bacterial endocarditis’ has been replaced by ‘Infective endocarditis’ (IE) since fungi are also involved as causative pathogens
IE is an uncommon but lifethreatening infection.
If the diagnosis is delayed or appropriate therapeutic measures postpone, mortality is still high
JADA, Vol. 138, 2007
European Heart Journal (2004) 00, 1-37
Guidelines AHA, Circulation. 2007;115:&NA;-.

3. INTRODUCTION
If untreated Infective Endocarditis (IE) is a fatal disease. Major diagnostic (first of all echocardiography) and therapeutic progress (mainly surgery during active IE) have contributed to some prognostic improvement.
In this respect, it is of utmost importance that:
IE is considered early in every patients with fever or septicaemia and cardiac murmurs.
Echocardiography is applied without delay in suspected IE.
Cardiologist, microbiologists and cardiac surgeons cooperate closely if IE is suspected or definite.

4. INTRODUCTION Recent data suggest it may be increasing,
In industrialized nations, patients are living longer
There is an increase in nosocomial infections
Intravenous drug use has increased in industrialized societies
Increasing application of cardiac surgery has provided new substrates for endocardial infection
The increased use of indwelling intravascular lines and implantable devices
the increased application of echocardiography
Cardiol Clin 21 (2003) 159–166

5. DEFINITION
IE is an endovascular, microbial infection of intracardiac structures facing the blood including infections of the large intrathoracic vesseis and of intracardiac foreign bodies.
The early characteristic lesion is a variably sized vegetation, although destruction, ulceration or abscess formation may be seen earlier by echocardiography.

6. Definition
Infectious Endocarditis (IE): an infection of the heart’s endocardial surface
Classified into four groups:
Native Valve IE
Prosthetic Valve IE
Intravenous drug abuse (IVDA) IE
Nosocomial IE

7. INFECTIVE ENDOCARDITIS
Characterized by inflammation or infection
two major predisposing factors:
susceptible cardiac or vascular substrate
lesions associated with high-velocity flow, jet impact and focal increases in the rate of shear
source of bacteremia

8. Further Classification
Acute
Affects normal heart valves
Rapidly destructive
Metastatic foci
Commonly Staph.
If not treated, usually fatal within 6 weeks
Subacute
Often affects damaged heart valves
Indolent nature
If not treated, usually fatal by one year

9. Pathophysiology
Turbulent blood flow disrupts the endocardium making it “sticky”
Bacteremia delivers the organisms to the endocardial surface
Adherence of the organisms to the endocardial surface
Eventual invasion of the valvular leaflets
IE often occurs when there is an underlying cardiac abnormality that creates a high-low pressure gradient.
The resultant turbulent blood flow disrupts the endocardial surface by peeling away the endothelium.
The body’s natural response to endothelial damage is to repair it by laying down a sticky platelet-fibrin meshwork, which is a nidus for infection.
Temporary bacteremia delivers the offending organism to the endocardial surface where is sticks to the platelet-fibrin meshwork. This festers into an infection that eventually invades the cardiac valves.
The pathophysiology is slightly different with IVDA. It has been postulated that repeated injections of drugs and particulate material causes microtrauma to the cardiac valves, thereby starting the infection cascade.

10. Proposed scheme for the pathogenesis of infective endocarditis
Mandell, Bennett, & Dolin:
Principles and Practice of Infectious Diseases, 6th ed

11. Epidemiology
Incidence difficult to ascertain and varies according to location
Much more common in males than in females
May occur in persons of any age and increasingly common in elderly
Mortality ranges from 20-30%
There is an estimated 10-15,000 new cases of IE diagnosed in the U.S. each year, although the exact incidence of IE is difficult to ascertain. IE is a relatively uncommon disease, is not a reportable disease, and different case definitions have existed throughout the years. Furthermore, the incidence varies greatly depending on geographic regions.
IE is more common among males. The male:female ratio varies from 2:1 to 9:1 depending on the source.
In the past, IE was a disease of children and young adults. It predominantly affected children with congenital heart disease and adults with rheumatic heart disease. Today, IE commonly affects the elderly, with almost 50% of cases in the U.S. occurring in patients over the age of 60. This may be due to the decreasing incidence of rheumatic heart disease and the increasing proportion of elderly in the U.S.
Mortality from IE remains high, and ranges from 20-30% despite newer antibiotics and surgical options.

12. Risk Factors Intravenous drug abuse
Artificial heart valves and pacemakers
Acquired heart defects
Calcific aortic stenosis
Mitral valve prolapse with regurgitation
Congenital heart defects
Intravascular catheters
The top three risk factors for IE include, IVDA, prosthetic heart valves, and structural heart disease.
IVDA – one large study of IVDAs found that the use of cocaine was associated with a higher risk of IE than other injectable drugs. The most significant risk factor for right-sided IE is IVDA, although left sided disease is quite common among IVDAs. The most common infecting organism is clearly S. aureus, particularly in right-sided infection.
Prosthetic valve IE comprises a small proportion of all cases of IE and occurs in only 1% of all patients with artificial heart valves. The greatest risk is in the first year following valve replacement.
Structural heart disease – approximately ¾ of all cases of IE occur in patients with preexisting structural heart abnormalities. The most common underlying heart abnormalities include mitral valve prolapse with mitral regurgitation and aortic stenosis.
The most common congenital heart defects include Tetralogy of Fallot, bicuspid aortic valves, coarctation of the aorta, VSDs, and patent ductus arteriosus. In general, the higher the gradient of the valvular insufficiency, the higher the risk of IE.
One of the greatest risk factors of all is a prior episode of IE. Some studies have documented recurrence as high as 9%.

13. Infecting Organisms Common bacteria Not so common bacteria S. aureus
Streptococci
Enterococci
Not so common bacteria
Fungi
Pseudomonas
HACEK
Staphlococcal and Streptococcal organisms comprise over 80% of all infecting organisms.

14. HACEK organisms
Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
Gram negative inhabitants of the upper airways.
Large vegetations, high likelihood of embolization.
Slow growing: hold cultures for 3 weeks.
Traditionally sensitive to beta lactams, now some produce beta lactamase.

15. Symptoms Acute Subacute High grade fever and chills
SOB (shortness of breath)
Arthralgias/ myalgias
Abdominal pain
Pleuritic chest pain
Back pain
Subacute
Low grade fever
Anorexia
Weight loss
Fatigue
Arthralgias/ myalgias
Abdominal pain
The onset of symptoms is usually ~2 weeks or less
from the initiating bacteremia

16. Signs Fever Heart murmur
Nonspecific signs – petechiae, subungal or “splinter” hemorrhages, clubbing, splenomegaly, neurologic changes
More specific signs - Osler’s Nodes, Janeway lesions, and Roth Spots

17. Petechiae Nonspecific Often located on extremities or mucous membranes
dermatology.about.com/.../
blpetechiaephoto.htm
Harden Library for the Health Sciences
hardin/
md/cdc/3184.html
Photo credit, Josh Fierer, M.D.
medicine.ucsd.edu/clinicalimg/ Eye-Petechiae.html

18. Splinter Hemorrhages Nonspecific Nonblanching
Subungal hemorrhages that extend the entire length of the nail or are primarily located at the proximal end of the nail (near the cuticle) are like due to trauma.
Nonspecific
Nonblanching
Linear reddish-brown lesions found under the nail bed
Usually do NOT extend the entire length of the nail

19. Osler’s Nodes More specific Painful and erythematous nodules
American College of Rheumatology
webrheum.bham.ac.uk/.../ default/pages/3b5.htm
Hand10/Hand10dx.html
More specific
Painful and erythematous nodules
Located on pulp of fingers and toes
More common in subacute IE

20. Janeway Lesions More specific Erythematous, blanching macules
Nonpainful
Located on palms and soles

21. The Essential Blood Test
Blood Cultures
Minimum of three blood cultures1
Three separate venipuncture sites
Obtain 10-20mL in adults and 0.5-5mL in children2
Positive Result
Typical organisms present in at least 2 separate samples
Persistently positive blood culture (atypical organisms)
Two positive blood cultures obtained at least 12 hours apart
Three or a more positive blood cultures in which the first and last samples were collected at least one hour apart
If you suspect the pt has subacute IE or is not critically ill, then the three samples can be collected over hours and antibiotics can be held until all three samples have been drawn.
However, if the pt is acutely ill, critical, or unstable, the three cultures should be obtained over a 1 hour time span before beginning empiric therapy.
There is no need to collect anaerobic blood cultures since virtually all cases of IE are caused by aerobic organisms.
There is little additional diagnostic yield to collecting more than three blood cultures unless the pt was previously on antibiotics. In one study of 206 cases of IE, the initial blood culture was positive in 96% of streptococcal IE and one of the first two cultures were positive 98% of the time. For pt’s with IE cause by organisms other than strep, one of the first two blood culture was positive in 100% of the cases.
The estimated diagnostic yield of a blood culture increases by about 3% per mL of blood cultured. One study found that the detection rate for bacteremia increased from 69% to 92% when at least 5mL of blood were used for culture.
The most common cause of negative cultures in patients with IE is prior antibiotic use.

22. Additional Labs CBC (complete blood count)
ESR (erythrocyte sedimentation rate) and CRP (C reactive protein)
Complement levels (C3, C4, CH50)
RF (rheumatoid factors)
Urinalysis
Baseline chemistries and coagulations
CBC – Look for a normochromic normocytic anemia and/or a leukocytosis.
ESR and CRP - Look for an elevated erythrocyte sedimentation rate and/or an elevated C-reactive protein which are present % of the time.
RF - Occasionally there will be an elevated levels of Rheumetoid Factor, particularly in patients who have been infected for six weeks or more. (Minor Duke’s Criteria)
UA - Urinalysis may reveal microscopic or gross hematuria, proteinuria, and pyuria. These findings along with a low serum complement level indicate a glomerulonephritis or “immunologic phenomena”. (Minor Duke’s Criteria)

23. Imaging Chest x-ray EKG Echocardiography
Look for multiple focal infiltrates and calcification of heart valves
EKG
Rarely diagnostic
Look for evidence of ischemia, conduction delay, and arrhythmias
Echocardiography
CXR – A chest xray can contain multiple diagnostic clues such as calcification of heart valves, which should raise suspicion in a febrile patient without an obvious source. More commonly, the chest xray may reveal septic pulmonary emboli in a patient with right-sided IE (Minor Duke’s Criteria).
EKG – An EKG alone cannot diagnose IE but it may show evidence of some of the disease’s complications. For example, EKG with ST changes may indicate ischemia or infarction from septic emboli. Arrhythmias such as heart block may indicated extension of the infection from the valves into the septum and surrounding cardiac tissue.

24. Indications for Echocardiography
Transthoracic echocardiography (TTE)
First line if suspected IE
Native valves
Transesophageal echocardiography (TEE)
Prosthetic valves
Intracardiac complications
Inadequate TTE
Fungal or S. aureus or bacteremia
TTE and TEE are complementary for evaluating cardiac hemodynamics and anatomy, but TEE has superior sensitivity, especially in detecting native valve vegetations, prosthetic valve vegetations, and local extension of infection. However, it is significantly more expensive and invasive.
If there is any suspicion of IE, get a TTE.
If there is staph or fungal bacteremia, a TEE should probably be obtained.
If there is a high clinical suspicion for IE and the TTE is negative, you should proceed to a TEE.
If there is a concern for intracardiac complications, a TEE is warranted.
It’s important to remember that the negative predictive value of a TEE is between 96-98%, meaning that a TEE cannot definitively rule out endocarditis. If the initial TEE is negative in a patient with a high clinical suspicion for IE, a repeat examiniation should be done if the pt does not improve.

25. Making the Diagnosis Pelletier and Petersdorf criteria (1977)
Classification scheme of definite, probable, and possible IE
Reasonably specific but lacked sensitivity
Von Reyn criteria (1981)
Added “rejected” as a category
Added more clinical criteria
Improved specificity and clinical utility
Duke criteria (1994)
Included the role of echocardiography in diagnosis
Added IVDA as a “predisposing heart condition”
Pelletier and Petersdorf criteria – 3 case categories:
Definite – histologic evidence of endocardial vegetations on examination of tissue
Probable - uniformly positive blood cultures with know underlying heart disease or embolic phenomena OR negative blood cultures in pts with fever, new regurgitant valvular heart murmur, and embolic phenomena
Possible - uniformly positive blood cultures with know underlying heart disease or embolic phenomena OR negative blood cultures with fever and known underlying heart disease and embolic phenomena
Von Reyn criteria – modified the above criteria to improve specificity and clinical utility.
Duke Criteria – relies upon major and minor clinical and pathologic criteria to classify cases as definite, possible, and rejected

26. Modified Duke Criteria
Definite IE
Microorganism (via culture or histology) in a valvular vegetation, embolized vegetation, or intracardiac abscess
Histologic evidence of vegetation or intracardiac abscess
Possible IE
2 major
1 major and 3 minor
5 minor
Rejected IE
Resolution of illness with four days or less of antibiotics
Multiple studies have validated the Duke criteria. When applied and reapplied over the entire evaluation, these criteria are sensitive and specific and very rarely erroneously reject a true endocarditis.

27. CRITERIA THAT SHOULD RAISE SUSPICION OF IE
High clinical suspicion (urgent indication for echocardiographic screening and possibly hospital admission)
New valve lesion/(regurgitant) murmur
Embolic events of unknown origin (esp. cerebral and renal infarction)
Sepsis of unknown origin
Haematuria, glomerulonephritis, and suspected renal infarction
“Fever “ plus
Prosthetic material inside the heart
Other high predispositions of IE
Newly developed ventricular arrhythmias or conduction disturbances
First manifestation of chronic heart failure
Positive blood cultures (if the organism identified is typical for NVE/PVE)
Cutaneous (Osler, janeway) or ophthalmic (roth) manifestations
Multifocal/rapid changing pulmonary infiltrations (right heart IE)
Peripheral abscesses (renal, spienic, spine) of unknown origin
Predisposition and recent diagnostic/therapeutic interventions known to result in significant bacteraemia
Low Clinical Suspicion
Fever plus none of the above

28. ECHOCARDIOGRAPHY
Any patient suspected of having Native Valve Endocarditis (NVE) by clinical criteria should be screened by Transthoracic Echocardiography (TTE).
When images are of good quality and prove to be negative and there is only a low clinical suspicion of IE, endocarditis is unlikely and other diagnosis are to be considered.
If suspicion of IE is high, TransEsophageal Echocardiography (TEE) should be performed in all TTE-negative cases, in suspected Prosthetic Valve Endocarditis (PVE), and if TTE is positive but complications are suspected or likely and before cardiac surgery during active IE.
If TEE remains negative and there is still suspicion, it should be repeated within one week. A repeatedly negative study should virtually exclude the diagnosis.

29. Three echocardiographic findings are considered to be major critetria in the diagnosis of IE:
A mobile, echodense mass attached to the valvular or the mural endocardium or to implanted prosthetic material
Demonstration of abscesses or fistulas
A new dehiscence of a valve prosthesis, especially when occurring late after implantation

30. Treatment Parenteral antibiotics Surgery Surveillance blood cultures
High serum concentrations to penetrate vegetations
Prolonged treatment to kill dormant bacteria clustered in vegetations
Surgery
Intracardiac complications
Surveillance blood cultures

31. ANTIMICROBIAL THERAPY
If initiation of antimicrobial therapy is urgent, empiric antibiotic treatment can be started thereafter (blood culture)
In all other cases it is recommended to post-pone therapy until blood cultures become positive.
Previous short term antibiotic  discontinue for at least 3 day before taking blood cultures.
Previous long term antibiotic treatment  discontinue for days.
ESC guideline; European Heart J 2004

32. 2 weeks regimen (combination) has similar cure rates to 4 week regimen
4 week regimen (monotherapy) preferred in
patients >65 yo
with 8th cranial nerve impairment
renal dysfunction
Cardiac/extracardiac abscess
Vancomycin only for patients not tolerate to penicillin / ceftriaxone
For combination antibiotics  given at same time or close together to increase synergistic effect

33. IE IN INTRAVENOUS DRUG USER (IVDU)
Most common: S aureus *, **
MRSA had been emerging (60-70% in Europe)**
Other organisms: P aeruginosa, Candida, enterococci, streptococci *, **
Polymicrobial infection 5-10% **
* AHA guidelines IE. Circulation 2005;111;e394-e433
** ESC guidelines Infective Endocarditis 2004

34. ANTIBIOTIC PROPHYLAXIS
Background for prophylaxis:
Bacteremia causes endocarditis
Viridans group streptococci are part of normal oral flora, and enterococci are part of normal GI and GU tract flora
These microorganisms were usually susceptible to antibiotics recommended for prophylaxis
Antibiotic prophylaxis prevents viridans group streptococcal or enterococcal experimental endocarditis in animals
AHA guideline: Prevention of Infective Endocarditis. Circulation 2007;115

35. Large number of poorly documented case reports implicated a dental procedure as a cause of IE
In some cases, there was a temporal relationship between a dental procedure and the onset of symptoms of IE
The risk of significant adverse reactions to an antibiotic is low in an individual patient
Morbidity and mortality from IE are high.

36. Cardiac condition in Which Antimicrobial Prophylaxis is Indicated
High Risk
Prosthetic heart valves
Complex congenital cyanotic heart diseases
Previous infective endocarditis
Surgically constructed systemic or pulmonary conduits
Moderate Risk
Acquired valvular heart disease
Mitral valve prolapse with valvular regurgitation or severe valve thickening
Non-cyanotic congenital heart diseases (except for secundum type Atrial Septal Defect) including bicuspid aortic valves
Hypertrophic cardiomyopathy

37. Predisposing diagnostic and therapeutic interventions
Procedure which may cause bacteraemia and for which antimicrobial prophylaxis is recommended
Diagnostic and therapeutic interventions likely to produce bacteraemia
Bronchoscopy (rigid instrument)
Cystoscopy during urinary tract infection
Biopsy of urinary tract/prostate
Dental procedures with the risk of gingival/mucosal trauma
Tonsillectomy and adenoidectomy
Oesophageal dilatation/ sclerotherapy
Instrumentation of obstructed biliary tracts
Transurethral resection of prostate
Urethral instrumentation/ dilation
Lithotripsy
Gynaecologic procedures in the presence of infection

38. New from AHA for IE prophylaxis
Bacteremia from daily activities (chewing food, tooth brushing and flossing, use of wooden toothpicks, use of water irrigation devices) is much more likely to cause IE than a dental procedure
Extremely small number of IE might be prevented by antibiotic prophylaxis, even if prophylaxis is 100% effective
AHA guideline: Prevention of Infective Endocarditis. Circulation 2007;115

39. Limit prophylaxis only to conditions with high adverse outcome from endocarditis
Maintenance of optimal oral health and hygiene may reduce the incidence of bacteremia from daily activities and is more important than prophylactic antibiotics
AHA guideline: Prevention of Infective Endocarditis. Circulation 2007;115

40. Complications Four etiologies Embolic Local spread of infection
Metastatic spread of infection
Formation of immune complexes – glomerulonephritis and arthritis

41. Embolic Complications
Occur in up to 40% of patients with IE
Predictors of embolization
Size of vegetation
Left-sided vegetations
Fungal pathogens, S. aureus, and Strep. Bovis
Incidence decreases significantly after initiation of effective antibiotics
Systemic emboli are among the most common complications of IE, occurring in up to 40% of patients. Subclinical emboli are often found on autopsy.

42. Embolic Complications
Stroke
Myocardial Infarction
Fragments of valvular vegetation or vegetation-induced stenosis of coronary ostia
Ischemic limbs
Hypoxia from pulmonary emboli
Abdominal pain (splenic or renal infarction)

43. Septic Pulmonary Emboli

44. Septic Retinal Embolus

45. Local Spread of Infection
Heart failure
Extensive valvular damage
Paravalvular abscess (30-40%)
Most common in aortic valve, IVDA, and S. aureus
May extend into adjacent conduction tissue causing arrythmias
Higher rates of embolization and mortality
Pericarditis
Fistulous intracardiac connections

46. Local Spread of Infection
Acute S. aureus IE with perforation of the
aortic valve and aortic valve vegetations.
Acute S. aureus IE with mitral valve ring
abscess extending into myocardium.

47. Metastatic Spread of Infection
Metastatic abscess
Kidneys, spleen, brain, soft tissues
Meningitis and/or encephalitis
Vertebral osteomyelitis
Septic arthritis

48. Poor Prognostic Factors
Female
S. aureus
Vegetation size
Aortic valve
Prosthetic valve
Older age
Diabetes mellitus
Low serum albumen
Apache II score
Heart failure
Paravalvular abscess
Embolic events

49. Summary IVDA and the elderly are at greatest risk of developing IE.
The signs and symptoms of IE are nonspecific and varied.
A thorough but timely evaluation (including serial blood cultures, adjunct labs, and an echo) is crucial to accurately diagnose and treat IE.
Beware of life-threatening complications.

50. THANK YOU

51. Faculty of Medicine Universitas Brawijaya Malang
ACUTE PERICARDITIS
Faculty of Medicine
Universitas Brawijaya
Malang

52. Incidence Exact incidence and prevalence are unknown
Diagnosed in 0.1% of hospitalized patients and 5% of patients admitted for non-acute MI chest pain
Observational study: 27.7 cases/100,000 population/year

54. Etiology: Can be Tricky. . .
Standard diagnostic evaluations are oftentimes relatively low yield
One series elucidated a cause in only 16% of patients
Leading possibilities:
Neoplasia
Tuberculosis
Non-tuberculous infection
Rheumatic disease

56. Initial clinical and echocardiographic evaluation of patients with suspected acute pericarditis

57. Diagnostic Criteria
Chest pain: anterior chest, sudden onset, pleuritic; may decrease in intensity when leans forward, may radiate to one or both trapezius ridges
Pericardial friction rub: most specific, heard best at LSB (Left sternal border)
EKG changes: new widespread ST elevation or PR depression
Pericardial effusion: absence of does not exclude diagnosis of pericarditis
Supporting signs/symptoms:
Elevated ESR (erythrocyte sedimentation rate), CRP (C reactive protein)
Fever
Leukocytosis

58. EKG
Electrocardiogram in acute pericarditis showing diffuse upsloping ST segment elevations seen best here in
leads II, III, aVF, and V2 to V6. There is also subtle PR segment deviation (positive in aVR, negative
in most other leads). ST segment elevation is due to a ventricular current of injury associated with epicardial
inflammation; similarly, the PR segment changes are due to an atrial current of injury which, in pericarditis,
typically displaces the PR segment upward in lead aVR and downward in most other leads.

59. Pericardial Effusion
Cardiomegaly due to a massive pericardial effusion. At least 200 mL of pericardial fluid must accumulate before the cardiac silhouette enlarges.

60. Tests EKG CXR PPD ANA HIV Blood cultures
Urgent echocardiogram if evidence of pericardial effusion
Not necessary:
Viral studies b/c yield is low and management is not altered

61. Treatment
NSAIDs + PPI
Aspirin (2-5 g/day)
Ibuprofen ( mg q6-8H)*
Ketorolac
Theoretical concern that anti-platelet agents promote development of hemorrhagic pericardial effusion has not been substantiated
Colchicine (0.5-1 mg/day) : may prevent recurrence
Glucocorticoids (prednisone 1 mg/kg/day): ? increased rate of complications. Should be restricted to:
Acute pericarditis due to connective tissue disease
Autoreactive (immune-mediated) pericarditis
Uremic pericarditis
*NSAID of choice unless associated with acute MI, where all non-ASA NSAIDs should be avoided

62. Prognosis for acute idiopathic pericarditis
Good long-term prognosis
Cardiac tamponade is rare, but up to 70% in cases with specific etiologies (eg. Neoplastic, tuberculous, purulent)
Constrictive pericarditis occurs in about 1% of patients
15-30% of patients not treated with colchicine develop either recurrent or incessant disease

63. Recurrent Pericarditis
Exact recurrence rate unknown
Most cases considered to be autoimmune
Risk Factors:
Lack of response to aspirin or other NSAID
Glucocorticoid therapy
Inappropriate pericardiotomy
Creation of a pericardial window
For some patients, symptoms can only be controlled with steroidal therapy

64. Autoreactive Pericarditis: diagnostic criteria
Pericardial fluid revealing >5000/mm3 mononuclear cells or antisarcolemmal antibodies
Inflammation in epicardial/endomyocardial biopsies by >14 cells/mm2
Exclusion of active viral infection both in pericardial effusion and endocardial/epicardial biopsies
Exclusion of tuberculosis, borrelia burgdorferi, chlamydia pneumoniae and other bacterial infection
Absence of neoplastic infiltration in effusion and biopsy samples
Exclusion of systemic, metabolic disorders and uremia

65. Treatment Aspirin NSAIDs
Colchicine: can reduce or eliminate need for glucocorticoids
Glucocorticoids: should be avoided unless required to treat patients who fail NSAID and colchicine therapy
Many believe that prednisone may perpetuate recurrences
Intrapericardial glucocorticoid therapy: sx improvement and prevention of recurrence in 90% of patients at 3 months and 84% at one year
Other immunosuppression
Azothoprine ( mg/day)
Cyclophosphamide
Mycophenolate: anecdotal evidence only
Methotrexate: limited data
IVIG: limited data
Pericardiectomy: To avoid poor wound healing, recommended to be off prednisone for one year. Reserved for the following cases:
If >1 recurrence is accompanied by tamponade
If recurrence is principally manifested by persistent pain despite an intensive medical trial and evidence of serious glucocorticoid toxicity

66. Thank You