Infective Endocarditis Faculty of Medicine University of Brawijaya Malang.
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Transcript of Infective Endocarditis Faculty of Medicine University of Brawijaya Malang.
Infective EndocarditisInfective Endocarditis
Faculty of Medicine Faculty of Medicine
University of BrawijayaUniversity of Brawijaya
MalangMalang
INTRODUCTIONINTRODUCTION
The term ‘bacterial endocarditis’ has been The term ‘bacterial endocarditis’ has been replaced by ‘Infective endocarditis’ (IE) since fungi replaced by ‘Infective endocarditis’ (IE) since fungi are also involved as causative pathogens are also involved as causative pathogens
IE is an uncommon but lifethreatening infection.IE is an uncommon but lifethreatening infection.
If the diagnosis is delayed or appropriate If the diagnosis is delayed or appropriate therapeutic measures postpone, mortality is still therapeutic measures postpone, mortality is still highhigh
JADA, Vol. 138, 2007JADA, Vol. 138, 2007European Heart Journal (2004) 00, 1-37European Heart Journal (2004) 00, 1-37
Guidelines AHA, Circulation. 2007;115:&NA;-.Guidelines AHA, Circulation. 2007;115:&NA;-.
If untreated Infective Endocarditis (IE) is a fatal If untreated Infective Endocarditis (IE) is a fatal disease. disease. Major diagnosticMajor diagnostic (first of all (first of all echocardiography) and echocardiography) and therapeutic progresstherapeutic progress (mainly surgery during active IE) have (mainly surgery during active IE) have contributed to some prognostic improvement.contributed to some prognostic improvement.In this respect, it is of utmost importance that:In this respect, it is of utmost importance that:– IE is considered early in every patients with fever or IE is considered early in every patients with fever or
septicaemia and cardiac murmurs.septicaemia and cardiac murmurs.– Echocardiography is applied without delay in Echocardiography is applied without delay in
suspected IE.suspected IE.– Cardiologist, microbiologists and cardiac surgeons Cardiologist, microbiologists and cardiac surgeons
cooperate closely if IE is suspected or definite.cooperate closely if IE is suspected or definite.
INTRODUCTIONINTRODUCTION
INTRODUCTIONINTRODUCTION
Cardiol Clin 21 (2003) 159–166Cardiol Clin 21 (2003) 159–166
Recent data suggest it may be increasing,Recent data suggest it may be increasing,1.1. In industrialized nations, patients are living longerIn industrialized nations, patients are living longer2.2. There is an increase in nosocomial infectionsThere is an increase in nosocomial infections3.3. Intravenous drug use has increased in industrialized Intravenous drug use has increased in industrialized
societiessocieties4.4. Increasing application of cardiac surgery has provided Increasing application of cardiac surgery has provided
new substrates for endocardial infectionnew substrates for endocardial infection5.5. The increased use of indwelling intravascular lines and The increased use of indwelling intravascular lines and
implantable devices implantable devices 6.6. the increased application of echocardiographythe increased application of echocardiography
IE is an IE is an endovascularendovascular, , microbial microbial infectioninfection of of intracardiac intracardiac structures facing structures facing the blood including infections of the large the blood including infections of the large intrathoracic vesseisintrathoracic vesseis and of and of intracardiac intracardiac foreign bodies.foreign bodies.The early characteristic lesion is a variably The early characteristic lesion is a variably sized vegetation, although destruction, sized vegetation, although destruction, ulceration or abscess formation may be ulceration or abscess formation may be seen earlier by echocardiography. seen earlier by echocardiography.
DEFINITIONDEFINITION
DefinitionDefinition
Infectious Endocarditis (IE):Infectious Endocarditis (IE): an infection of an infection of the heart’s endocardial surfacethe heart’s endocardial surface
Classified into Classified into fourfour groups: groups: – Native Valve IENative Valve IE– Prosthetic Valve IEProsthetic Valve IE– Intravenous drug abuse (IVDA) IEIntravenous drug abuse (IVDA) IE– Nosocomial IENosocomial IE
Characterized byCharacterized by inflammation inflammation or or infectioninfection
two major predisposing factors:two major predisposing factors:– susceptible susceptible cardiac cardiac or or vascular vascular substratesubstrate
lesions associated with high-velocity flow, jet impact and lesions associated with high-velocity flow, jet impact and focal increases in the rate of shearfocal increases in the rate of shear
– source of source of bacteremiabacteremia
INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
Further ClassificationFurther Classification
AcuteAcute– Affects normal heart Affects normal heart
valvesvalves– Rapidly destructiveRapidly destructive– Metastatic fociMetastatic foci– Commonly Staph.Commonly Staph.– If not treated, usually If not treated, usually
fatal within 6 weeksfatal within 6 weeks
SubacuteSubacute– Often affects damaged Often affects damaged
heart valvesheart valves– Indolent natureIndolent nature– If not treated, usually If not treated, usually
fatal by one yearfatal by one year
PathophysiologyPathophysiology
1.1. Turbulent blood flow Turbulent blood flow disrupts the disrupts the endocardium making it “sticky”endocardium making it “sticky”
2.2. Bacteremia Bacteremia delivers the organisms to delivers the organisms to the endocardial surface the endocardial surface
3.3. AdherenceAdherence of the organisms to the of the organisms to the endocardial surfaceendocardial surface
4.4. Eventual invasionEventual invasion of the valvular of the valvular leafletsleaflets
Mandell, Bennett, & Dolin:
Principles and Practice of Infectious Diseases, 6th ed
Proposed scheme for the pathogenesis of infective endocarditis
EpidemiologyEpidemiology
Incidence difficult to ascertain and varies Incidence difficult to ascertain and varies according to locationaccording to location
Much more common in males than in Much more common in males than in femalesfemales
May occur in persons of any age and May occur in persons of any age and increasingly common in elderlyincreasingly common in elderly
Mortality ranges from 20-30%Mortality ranges from 20-30%
Risk FactorsRisk Factors
Intravenous drug abuseIntravenous drug abuse
Artificial heart valves and pacemakers Artificial heart valves and pacemakers
Acquired heart defectsAcquired heart defects– Calcific aortic stenosisCalcific aortic stenosis– Mitral valve prolapse with regurgitationMitral valve prolapse with regurgitation
Congenital heart defectsCongenital heart defects
Intravascular cathetersIntravascular catheters
Infecting OrganismsInfecting Organisms
Common bacteriaCommon bacteria– S. aureusS. aureus– Streptococci Streptococci – EnterococciEnterococci
Not so common bacteriaNot so common bacteria– FungiFungi– PseudomonasPseudomonas– HACEKHACEK
HACEK organismsHACEK organisms
• Hemophilus, Actinobacillus, Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, KingellaCardiobacterium, Eikenella, Kingella
• Gram negative inhabitants of the upper Gram negative inhabitants of the upper airways.airways.
• Large vegetations, high likelihood of Large vegetations, high likelihood of embolization.embolization.
• Slow growing: hold cultures for 3 weeks.Slow growing: hold cultures for 3 weeks.• Traditionally sensitive to beta lactams, now Traditionally sensitive to beta lactams, now
some produce beta lactamase.some produce beta lactamase.
SymptomsSymptoms
AcuteAcute– High grade fever and High grade fever and
chillschills– SOBSOB (shortness of (shortness of
breath)breath)– Arthralgias/ myalgiasArthralgias/ myalgias– Abdominal painAbdominal pain– Pleuritic chest painPleuritic chest pain– Back painBack pain
SubacuteSubacute– Low grade feverLow grade fever– AnorexiaAnorexia– Weight lossWeight loss– FatigueFatigue– Arthralgias/ myalgiasArthralgias/ myalgias– Abdominal painAbdominal pain
The onset of symptoms is usually ~2 weeks or less from the initiating bacteremia
SignsSignsFever Fever
Heart murmurHeart murmur
Nonspecific signs – petechiae, subungal Nonspecific signs – petechiae, subungal or “splinter” hemorrhages, clubbing, or “splinter” hemorrhages, clubbing, splenomegaly, neurologic changessplenomegaly, neurologic changes
More specific signs - Osler’s Nodes, More specific signs - Osler’s Nodes, Janeway lesions, and Roth SpotsJaneway lesions, and Roth Spots
PetechiaePetechiae
Photo credit, Josh Fierer, M.D. medicine.ucsd.edu/clinicalimg/ Eye-Petechiae.html
Harden Library for the Health Scienceswww.lib.uiowa.edu/ hardin/md/cdc/3184.html
1. Nonspecific2. Often located on extremities
or mucous membranesdermatology.about.com/.../ blpetechiaephoto.htm
Splinter HemorrhagesSplinter Hemorrhages
1. Nonspecific2. Nonblanching3. Linear reddish-brown lesions found under the nail bed4. Usually do NOT extend the entire length of the nail
Osler’s NodesOsler’s Nodes
1. More specific2. Painful and erythematous nodules3. Located on pulp of fingers and toes4. More common in subacute IE
American College of Rheumatologywebrheum.bham.ac.uk/.../ default/pages/3b5.htm www.meddean.luc.edu/.../
Hand10/Hand10dx.html
Janeway LesionsJaneway Lesions
1. More specific2. Erythematous, blanching macules 3. Nonpainful4. Located on palms and soles
TheThe EssentialEssential Blood TestBlood Test
Blood CulturesBlood Cultures– Minimum of three blood culturesMinimum of three blood cultures11
– Three separate venipuncture sitesThree separate venipuncture sites– Obtain 10-20mL in adults and 0.5-5mL in childrenObtain 10-20mL in adults and 0.5-5mL in children22
Positive ResultPositive Result– Typical organisms present in at least Typical organisms present in at least 22 separate samples separate samples– Persistently positive blood culture (atypical organisms)Persistently positive blood culture (atypical organisms)
Two positive blood cultures obtained at least 12 hours apartTwo positive blood cultures obtained at least 12 hours apartThree or a more positive blood cultures in which the first and Three or a more positive blood cultures in which the first and last samples were collected at least one hour apartlast samples were collected at least one hour apart
Additional LabsAdditional Labs
CBCCBC (complete blood count) (complete blood count)
ESRESR (erythrocyte sedimentation rate) and (erythrocyte sedimentation rate) and CRPCRP (C reactive protein) (C reactive protein)
Complement levels (C3, C4, CH50)Complement levels (C3, C4, CH50)
RFRF (rheumatoid factors) (rheumatoid factors)
UrinalysisUrinalysis
Baseline chemistries and coagBaseline chemistries and coagulationulationss
ImagingImaging
Chest x-ray Chest x-ray – Look for multiple focal infiltrates and Look for multiple focal infiltrates and
calcification of heart valvescalcification of heart valves
EKGEKG– Rarely diagnosticRarely diagnostic– Look for evidence of ischemia, conduction Look for evidence of ischemia, conduction
delay, and arrhythmiasdelay, and arrhythmias
EchocardiographyEchocardiography
Indications for EchocardiographyIndications for Echocardiography
Transthoracic echocardiography (TTE)Transthoracic echocardiography (TTE)– First line if suspected IEFirst line if suspected IE– Native valvesNative valves
Transesophageal echocardiography (TEE)Transesophageal echocardiography (TEE)– Prosthetic valvesProsthetic valves– Intracardiac complicationsIntracardiac complications– Inadequate TTE Inadequate TTE – Fungal or S. aureus or bacteremiaFungal or S. aureus or bacteremia
Making the DiagnosisMaking the Diagnosis
Pelletier and Petersdorf criteriaPelletier and Petersdorf criteria (1977) (1977)– Classification scheme of definite, probable, and possible IEClassification scheme of definite, probable, and possible IE
– Reasonably specific but lacked sensitivityReasonably specific but lacked sensitivity
Von Reyn criteriaVon Reyn criteria (1981) (1981)– Added “rejected” as a categoryAdded “rejected” as a category
– Added more clinical criteriaAdded more clinical criteria
– Improved specificity and clinical utilityImproved specificity and clinical utility
Duke criteriaDuke criteria (1994) (1994)– Included the role of echocardiography in diagnosisIncluded the role of echocardiography in diagnosis
– Added IVDA as a “predisposing heart condition”Added IVDA as a “predisposing heart condition”
Modified Duke CriteriaModified Duke Criteria
Definite IEDefinite IE– Microorganism (via culture or histology) in a valvular vegetation, Microorganism (via culture or histology) in a valvular vegetation,
embolized vegetation, or intracardiac abscessembolized vegetation, or intracardiac abscess– Histologic evidence of vegetation or intracardiac abscessHistologic evidence of vegetation or intracardiac abscess
Possible IEPossible IE– 2 major2 major– 1 major and 3 minor1 major and 3 minor– 5 minor5 minor
Rejected IERejected IE– Resolution of illness with four days or less of antibioticsResolution of illness with four days or less of antibiotics
High clinical suspicion (urgent indication for echocardiographic High clinical suspicion (urgent indication for echocardiographic screening and possibly hospital admission)screening and possibly hospital admission)– New valve lesion/(regurgitant) murmurNew valve lesion/(regurgitant) murmur– Embolic events of unknown origin (esp. cerebral and renal infarction)Embolic events of unknown origin (esp. cerebral and renal infarction)– Sepsis of unknown origin Sepsis of unknown origin – Haematuria, glomerulonephritis, and suspected renal infarctionHaematuria, glomerulonephritis, and suspected renal infarction– ““Fever “ plusFever “ plus
Prosthetic material inside the heart Prosthetic material inside the heart Other high predispositions of IEOther high predispositions of IENewly developed ventricular arrhythmias or conduction disturbancesNewly developed ventricular arrhythmias or conduction disturbancesFirst manifestation of chronic heart failureFirst manifestation of chronic heart failurePositive blood cultures (if the organism identified is typical for NVE/PVE)Positive blood cultures (if the organism identified is typical for NVE/PVE)Cutaneous (Osler, janeway) or ophthalmic (roth) manifestationsCutaneous (Osler, janeway) or ophthalmic (roth) manifestationsMultifocal/rapid changing pulmonary infiltrations (right heart IE)Multifocal/rapid changing pulmonary infiltrations (right heart IE)Peripheral abscesses (renal, spienic, spine) of unknown originPeripheral abscesses (renal, spienic, spine) of unknown originPredisposition and recent diagnostic/therapeutic interventions known to Predisposition and recent diagnostic/therapeutic interventions known to result in significant bacteraemia result in significant bacteraemia
Low Clinical Suspicion Low Clinical Suspicion – Fever plus none of the aboveFever plus none of the above
CRITERIA THAT SHOULD RAISE CRITERIA THAT SHOULD RAISE SUSPICION OF IESUSPICION OF IE
Any patient suspected of having Native Valve Endocarditis (NVE) by Any patient suspected of having Native Valve Endocarditis (NVE) by clinical criteria clinical criteria should be screened by Transthoracic should be screened by Transthoracic Echocardiography (TTE).Echocardiography (TTE).
When images are of When images are of good qualitygood quality and and prove to be negativeprove to be negative and and there is only a low clinical suspicion of IE, endocarditis is unlikely there is only a low clinical suspicion of IE, endocarditis is unlikely and other diagnosis are to be considered.and other diagnosis are to be considered.
If suspicion of IE is high, TransEsophageal Echocardiography (TEE) If suspicion of IE is high, TransEsophageal Echocardiography (TEE) should be performed in all should be performed in all TTE-negative casesTTE-negative cases, in , in suspected suspected Prosthetic Valve Endocarditis (PVE),Prosthetic Valve Endocarditis (PVE), and if and if TTE is positive but TTE is positive but complications are suspectedcomplications are suspected or likely and or likely and before cardiac before cardiac surgery during active IE.surgery during active IE.
If TEE remains negative and there is still suspicion, it should be If TEE remains negative and there is still suspicion, it should be repeated within repeated within one weekone week. A repeatedly negative study should . A repeatedly negative study should virtually exclude the diagnosis.virtually exclude the diagnosis.
ECHOCARDIOGRAPHYECHOCARDIOGRAPHY
Three echocardiographic findingsThree echocardiographic findings are are considered to be major critetria in the considered to be major critetria in the diagnosis of IE:diagnosis of IE:– A mobile, echodense mass attached to the A mobile, echodense mass attached to the
valvular or the mural endocardium or to valvular or the mural endocardium or to implanted prosthetic materialimplanted prosthetic material
– Demonstration of abscesses or fistulasDemonstration of abscesses or fistulas– A new dehiscence of a valve prosthesis, A new dehiscence of a valve prosthesis,
especially when occurring late after especially when occurring late after implantationimplantation
TreatmentTreatment
Parenteral antibioticsParenteral antibiotics– High serum concentrations to penetrate High serum concentrations to penetrate
vegetationsvegetations– Prolonged treatment to kill dormant bacteria Prolonged treatment to kill dormant bacteria
clustered in vegetationsclustered in vegetations
SurgerySurgery– Intracardiac complicationsIntracardiac complications
Surveillance blood culturesSurveillance blood cultures
If initiation of antimicrobial therapy is urgent,If initiation of antimicrobial therapy is urgent, empiric antibiotic treatmentempiric antibiotic treatment can be started can be started thereafter (blood culture) thereafter (blood culture) In all other cases it is recommended to post-In all other cases it is recommended to post-pone therapy until blood cultures become pone therapy until blood cultures become positive.positive.
Previous short term antibiotic Previous short term antibiotic discontinue for discontinue for at least 3 day before taking blood cultures.at least 3 day before taking blood cultures.
Previous long term antibiotic treatment Previous long term antibiotic treatment discontinue for 6 - 7 days.discontinue for 6 - 7 days.
ESC guideline; European Heart J 2004
ANTIMICROBIAL THERAPYANTIMICROBIAL THERAPY
2 weeks regimen (combination) has similar 2 weeks regimen (combination) has similar cure rates to 4 week regimencure rates to 4 week regimen4 week regimen (monotherapy) preferred in 4 week regimen (monotherapy) preferred in – patients >65 yo patients >65 yo – with 8with 8thth cranial nerve impairment cranial nerve impairment– renal dysfunction renal dysfunction – Cardiac/extracardiac abscessCardiac/extracardiac abscess
Vancomycin only for patients not tolerate to Vancomycin only for patients not tolerate to penicillin / ceftriaxonepenicillin / ceftriaxoneFor combination antibiotics For combination antibiotics given at given at same time or close together to increase same time or close together to increase synergistic effectsynergistic effect
Most common: Most common: S aureus *, **S aureus *, **
MRSA had been emerging (60-70% in MRSA had been emerging (60-70% in Europe)**Europe)**
Other organisms: Other organisms: P aeruginosaP aeruginosa, , CandidaCandida, , enterococci, streptococci *, **enterococci, streptococci *, **
Polymicrobial infection 5-10% **Polymicrobial infection 5-10% **
* AHA guidelines IE. Circulation 2005;111;e394-e433
** ESC guidelines Infective Endocarditis 2004
IE IN INTRAVENOUS DRUG USER IE IN INTRAVENOUS DRUG USER (IVDU)(IVDU)
Background for prophylaxis:Background for prophylaxis:
– Bacteremia causes endocarditis Bacteremia causes endocarditis
– Viridans group streptococci are part of normal oral flora, Viridans group streptococci are part of normal oral flora, and enterococci are part of normal GI and GU tract and enterococci are part of normal GI and GU tract floraflora
– These microorganisms were usually susceptible to These microorganisms were usually susceptible to
antibiotics recommended for prophylaxis antibiotics recommended for prophylaxis
– Antibiotic prophylaxis prevents viridans group Antibiotic prophylaxis prevents viridans group streptococcal or enterococcal experimental endocarditis streptococcal or enterococcal experimental endocarditis in animalsin animals
AHA guideline: Prevention of Infective Endocarditis. Circulation 2007;115
ANTIBIOTIC PROPHYLAXISANTIBIOTIC PROPHYLAXIS
– Large number of poorly documented case Large number of poorly documented case reports implicated a dental procedure as a reports implicated a dental procedure as a cause of IE cause of IE
– In some cases, there was a temporal In some cases, there was a temporal relationship between a dental procedure and relationship between a dental procedure and the onset of symptoms of IE the onset of symptoms of IE
– The risk of significant adverse reactions to an The risk of significant adverse reactions to an antibiotic is low in an individual patientantibiotic is low in an individual patient
– Morbidity and mortality from IE are high.Morbidity and mortality from IE are high.
High RiskHigh Risk– Prosthetic heart valvesProsthetic heart valves– Complex congenital cyanotic heart diseasesComplex congenital cyanotic heart diseases– Previous infective endocarditisPrevious infective endocarditis– Surgically constructed systemic or pulmonary Surgically constructed systemic or pulmonary
conduitsconduits
Moderate RiskModerate Risk– Acquired valvular heart diseaseAcquired valvular heart disease– Mitral valve prolapse with valvular regurgitation or Mitral valve prolapse with valvular regurgitation or
severe valve thickeningsevere valve thickening– Non-cyanotic congenital heart diseases (except for Non-cyanotic congenital heart diseases (except for
secundum type Atrial Septal Defect) including secundum type Atrial Septal Defect) including bicuspid aortic valves bicuspid aortic valves
– Hypertrophic cardiomyopathy Hypertrophic cardiomyopathy
Cardiac condition in Which Antimicrobial Prophylaxis is Indicated
Procedure which may cause bacteraemia and for which Procedure which may cause bacteraemia and for which antimicrobial prophylaxis is recommendedantimicrobial prophylaxis is recommendedDiagnostic and therapeutic interventions likely to produce Diagnostic and therapeutic interventions likely to produce bacteraemiabacteraemia– Bronchoscopy (rigid instrument)Bronchoscopy (rigid instrument)– Cystoscopy during urinary tract infectionCystoscopy during urinary tract infection– Biopsy of urinary tract/prostateBiopsy of urinary tract/prostate– Dental procedures with the risk of gingival/mucosal traumaDental procedures with the risk of gingival/mucosal trauma– Tonsillectomy and adenoidectomyTonsillectomy and adenoidectomy– Oesophageal dilatation/ sclerotherapyOesophageal dilatation/ sclerotherapy– Instrumentation of obstructed biliary tractsInstrumentation of obstructed biliary tracts– Transurethral resection of prostateTransurethral resection of prostate– Urethral instrumentation/ dilationUrethral instrumentation/ dilation– LithotripsyLithotripsy– Gynaecologic procedures in the presence of infection Gynaecologic procedures in the presence of infection
Predisposing diagnostic and therapeutic interventions
Bacteremia from daily activities (chewing food, Bacteremia from daily activities (chewing food, tooth brushing and flossing, use of wooden tooth brushing and flossing, use of wooden toothpicks, use of water irrigation devices) is toothpicks, use of water irrigation devices) is much more likely to cause IE than a dental much more likely to cause IE than a dental procedureprocedure
Extremely small number of IE might be Extremely small number of IE might be prevented by antibiotic prophylaxis, even if prevented by antibiotic prophylaxis, even if prophylaxis is 100% effectiveprophylaxis is 100% effective
AHA guideline: Prevention of Infective Endocarditis. Circulation 2007;115
New from AHA for IE prophylaxis
Limit prophylaxis Limit prophylaxis only to conditions with only to conditions with high adverse outcome from endocarditishigh adverse outcome from endocarditis
Maintenance of optimal Maintenance of optimal oral health and oral health and hygienehygiene may reduce the incidence of may reduce the incidence of bacteremia from daily activities and is bacteremia from daily activities and is mmore importantore important than prophylactic than prophylactic antibioticsantibiotics
AHA guideline: Prevention of Infective Endocarditis. Circulation 2007;115
ComplicationsComplications
Four etiologiesFour etiologies– EmbolicEmbolic– Local spread of infectionLocal spread of infection– Metastatic spread of infectionMetastatic spread of infection– Formation of immune complexes – Formation of immune complexes –
glomerulonephritis and arthritisglomerulonephritis and arthritis
Embolic ComplicationsEmbolic Complications
Occur in up to 40% of patients with IEOccur in up to 40% of patients with IE
Predictors of embolizationPredictors of embolization– Size of vegetationSize of vegetation– Left-sided vegetationsLeft-sided vegetations– Fungal pathogens, S. aureus, and Strep. Fungal pathogens, S. aureus, and Strep.
BovisBovis
Incidence decreases significantly after Incidence decreases significantly after initiation of effective antibioticsinitiation of effective antibiotics
Embolic ComplicationsEmbolic Complications
StrokeStroke
Myocardial InfarctionMyocardial Infarction– Fragments of valvular vegetation or Fragments of valvular vegetation or
vegetation-induced stenosis of coronary ostiavegetation-induced stenosis of coronary ostia
Ischemic limbsIschemic limbs
Hypoxia from pulmonary emboliHypoxia from pulmonary emboli
Abdominal pain (splenic or renal infarction) Abdominal pain (splenic or renal infarction)
Septic Pulmonary EmboliSeptic Pulmonary Emboli
http://www.emedicine.com/emerg/topic164.htm
Septic Retinal EmbolusSeptic Retinal Embolus
Local Spread of InfectionLocal Spread of Infection
Heart failureHeart failure– Extensive valvular damageExtensive valvular damage
Paravalvular abscessParavalvular abscess (30-40%) (30-40%)– Most common in aortic valve, IVDA, and S. aureusMost common in aortic valve, IVDA, and S. aureus– May extend into adjacent conduction tissue causing May extend into adjacent conduction tissue causing
arrythmiasarrythmias– Higher rates of embolization and mortalityHigher rates of embolization and mortality
PericarditisPericarditis
Fistulous intracardiac connectionsFistulous intracardiac connections
Local Spread of InfectionLocal 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.
Metastatic Spread of InfectionMetastatic Spread of Infection
Metastatic abscess Metastatic abscess – Kidneys, spleen, brain, soft tissuesKidneys, spleen, brain, soft tissues
Meningitis and/or encephalitisMeningitis and/or encephalitis
Vertebral osteomyelitisVertebral osteomyelitis
Septic arthritisSeptic arthritis
Poor Prognostic FactorsPoor Prognostic Factors
FemaleFemale
S. aureusS. aureus
Vegetation sizeVegetation size
Aortic valve Aortic valve
Prosthetic valveProsthetic valve
Older ageOlder age
Diabetes mellitusDiabetes mellitus
Low serum albumen Low serum albumen
Apache II scoreApache II score
Heart failureHeart failure
Paravalvular abscessParavalvular abscess
Embolic eventsEmbolic events
SummarySummary
IVDA and the elderly are at greatest risk of IVDA and the elderly are at greatest risk of developing IE.developing IE.The signs and symptoms of IE are The signs and symptoms of IE are nonspecific and varied.nonspecific and varied.A thorough but timely evaluation (including A thorough but timely evaluation (including serial blood cultures, adjunct labs, and an serial blood cultures, adjunct labs, and an echo) is crucial to accurately diagnose and echo) is crucial to accurately diagnose and treat IE.treat IE.Beware of life-threatening complications.Beware of life-threatening complications.
THANK YOUTHANK YOU
ACUTE ACUTE PERICARDITISPERICARDITIS
Faculty of MedicineFaculty of Medicine
Universitas BrawijayaUniversitas Brawijaya
MalangMalang
IncidenceIncidence
Exact incidence and prevalence are Exact incidence and prevalence are unknownunknown
Diagnosed in 0.1% of hospitalized Diagnosed in 0.1% of hospitalized patients and 5% of patients admitted for patients and 5% of patients admitted for non-acute MI chest painnon-acute MI chest pain
Observational study: 27.7 cases/100,000 Observational study: 27.7 cases/100,000 population/yearpopulation/year
Etiology: Can be Tricky. . . Etiology: Can be Tricky. . .
Standard diagnostic evaluations are Standard diagnostic evaluations are oftentimes relatively low yieldoftentimes relatively low yield
One series elucidated a cause in only 16% One series elucidated a cause in only 16% of patientsof patients
Leading possibilities: Leading possibilities: – NeoplasiaNeoplasia– TuberculosisTuberculosis– Non-tuberculous infectionNon-tuberculous infection– Rheumatic diseaseRheumatic disease
Initial clinical and echocardiographic Initial clinical and echocardiographic evaluation of patients with suspected acute evaluation of patients with suspected acute
pericarditis pericarditis
Diagnostic CriteriaDiagnostic Criteria
Chest pain: anterior chest, sudden onset, pleuritic; Chest pain: anterior chest, sudden onset, pleuritic; may decrease in intensity when leans forward, may may decrease in intensity when leans forward, may radiate to one or both trapezius ridgesradiate to one or both trapezius ridges
Pericardial friction rub: most specific, heard best at Pericardial friction rub: most specific, heard best at LSB (Left sternal border)LSB (Left sternal border)
EKG changes: new widespread ST elevation or PR EKG changes: new widespread ST elevation or PR depressiondepression
Pericardial effusion: absence of does not exclude Pericardial effusion: absence of does not exclude diagnosis of pericarditisdiagnosis of pericarditis
Supporting signs/symptoms:Supporting signs/symptoms: Elevated ESR (erythrocyte sedimentation rate), CRP (C Elevated ESR (erythrocyte sedimentation rate), CRP (C
reactive protein)reactive protein) FeverFever LeukocytosisLeukocytosis
EKGEKG
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.
Pericardial EffusionPericardial Effusion
Cardiomegaly due to a massive pericardial effusion. At least 200 mL of pericardial fluid must accumulate before the cardiac silhouette enlarges.
TestsTests
EKGEKG CXRCXR PPDPPD ANAANA HIVHIV Blood culturesBlood cultures Urgent echocardiogram if evidence of pericardial Urgent echocardiogram if evidence of pericardial
effusioneffusion Not necessary: Not necessary:
Viral studies b/c yield is low and management is not Viral studies b/c yield is low and management is not alteredaltered
TreatmentTreatment
NSAIDs + PPINSAIDs + PPI Aspirin (2-5 g/day)Aspirin (2-5 g/day) Ibuprofen (300-800 mg q6-8H)* Ibuprofen (300-800 mg q6-8H)* KetorolacKetorolac
Theoretical concern that anti-platelet agents promote development of Theoretical concern that anti-platelet agents promote development of hemorrhagic pericardial effusion has not been substantiatedhemorrhagic pericardial effusion has not been substantiated
Colchicine (0.5-1 mg/day) : may prevent recurrenceColchicine (0.5-1 mg/day) : may prevent recurrence Glucocorticoids (prednisone 1 mg/kg/day): ? increased rate of Glucocorticoids (prednisone 1 mg/kg/day): ? increased rate of
complications. Should be restricted to:complications. Should be restricted to: Acute pericarditis due to connective tissue diseaseAcute pericarditis due to connective tissue disease Autoreactive (immune-mediated) pericarditisAutoreactive (immune-mediated) pericarditis Uremic pericarditisUremic pericarditis
*NSAID of choice unless associated with acute MI, where all non-ASA NSAIDs should be avoided
Prognosis for acute idiopathic Prognosis for acute idiopathic pericarditispericarditis
Good long-term prognosisGood long-term prognosis
Cardiac tamponade is rare, but up to 70% Cardiac tamponade is rare, but up to 70% in cases with specific etiologies (eg. in cases with specific etiologies (eg. Neoplastic, tuberculous, purulent)Neoplastic, tuberculous, purulent)
Constrictive pericarditis occurs in about 1% Constrictive pericarditis occurs in about 1% of patientsof patients
15-30% of patients not treated with 15-30% of patients not treated with colchicine develop either recurrent or colchicine develop either recurrent or incessant diseaseincessant disease
Recurrent PericarditisRecurrent Pericarditis
Exact recurrence rate unknownExact recurrence rate unknown
Most cases considered to be autoimmuneMost cases considered to be autoimmune
Risk Factors:Risk Factors:– Lack of response to aspirin or other NSAIDLack of response to aspirin or other NSAID– Glucocorticoid therapyGlucocorticoid therapy– Inappropriate pericardiotomyInappropriate pericardiotomy– Creation of a pericardial windowCreation of a pericardial window
For some patients, symptoms can only be For some patients, symptoms can only be controlled with steroidal therapycontrolled with steroidal therapy
Autoreactive Pericarditis:Autoreactive Pericarditis: diagnostic criteria diagnostic criteria
Pericardial fluid revealing >5000/mm3 mononuclear Pericardial fluid revealing >5000/mm3 mononuclear cells or antisarcolemmal antibodiescells or antisarcolemmal antibodies
Inflammation in epicardial/endomyocardial biopsies Inflammation in epicardial/endomyocardial biopsies by >14 cells/mm2by >14 cells/mm2
Exclusion of active viral infection both in pericardial Exclusion of active viral infection both in pericardial effusion and endocardial/epicardial biopsieseffusion and endocardial/epicardial biopsies
Exclusion of tuberculosis, borrelia burgdorferi, Exclusion of tuberculosis, borrelia burgdorferi, chlamydia pneumoniae and other bacterial infection chlamydia pneumoniae and other bacterial infection
Absence of neoplastic infiltration in effusion and Absence of neoplastic infiltration in effusion and biopsy samplesbiopsy samples
Exclusion of systemic, metabolic disordersExclusion of systemic, metabolic disorders and and uremiauremia
Treatment Treatment
AspirinAspirin NSAIDsNSAIDs Colchicine: can reduce or eliminate need for glucocorticoidsColchicine: can reduce or eliminate need for glucocorticoids Glucocorticoids: should be avoided unless required to treat patients Glucocorticoids: should be avoided unless required to treat patients
who fail NSAID and colchicine therapywho fail NSAID and colchicine therapy Many believe that prednisone may perpetuate recurrencesMany believe that prednisone may perpetuate recurrences Intrapericardial glucocorticoid therapy: sx improvement and prevention Intrapericardial glucocorticoid therapy: sx improvement and prevention
of recurrence in 90% of patients at 3 months and 84% at one yearof recurrence in 90% of patients at 3 months and 84% at one year Other immunosuppressionOther immunosuppression
Azothoprine (75-100 mg/day)Azothoprine (75-100 mg/day) CyclophosphamideCyclophosphamide Mycophenolate: anecdotal evidence onlyMycophenolate: anecdotal evidence only Methotrexate: limited dataMethotrexate: limited data IVIG: limited dataIVIG: limited data
Pericardiectomy: To avoid poor wound healing, recommended to be Pericardiectomy: To avoid poor wound healing, recommended to be off prednisone for one year. Reserved for the following cases:off prednisone for one year. Reserved for the following cases: If >1 recurrence is accompanied by tamponadeIf >1 recurrence is accompanied by tamponade If recurrence is principally manifested by persistent pain despite an If recurrence is principally manifested by persistent pain despite an
intensive medical trial and evidence of serious glucocorticoid toxicityintensive medical trial and evidence of serious glucocorticoid toxicity